TY  - JOUR
AU  - Jovanović, Ivan G.
AU  - Živković, Maja
AU  - Đurić, Tamara
AU  - Stojković, Ljiljana S.
AU  - Ješić, Snežana
AU  - Stanković, Aleksandra
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8684
AB  - Objectives/Hypothesis: To establish comprehensive transcriptomic profiles of cholesteatoma perimatrix tissue and granulation tissue from chronic otitis media (COM) that did not develop cholesteatoma, which can indicate molecular pathways involved in the cholesteatoma perimatrix pathology and invasiveness. Study Design: Retrospective Case Series. Methods: Transcriptome data were obtained from cholesteatoma perimatrix tissue and COM granulation tissue by an Illumina iScan microarray. Differentially expressed genes (DEGs) were subsequently analyzed using both bioinformatical functional annotation and network analysis. Expression of candidate genes (MMP9 and LCN2) was validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) on a larger group of samples. Results: Analysis of the transcriptome led to the identification of 169 differentially expressed genes between investigated tissues. Bioinformatic analysis suggested that most significant biological processes involving DEGs were previously described in cholesteatoma pathology. Network analysis identified ERBB2, TFAP2A, and TP63 as major hubs of the DEGs molecular network. Furthermore, it was observed that the cellular component most significantly enriched in DEGs was extracellular space containing 47 DEGs. Using qRT-PCR, it was confirmed that mRNA levels of the major extracellular hub (MMP9) are increased, whereas its interacting molecule (LCN2) mRNA levels were decreased in cholesteatoma perimatrix tissue compared to COM granulation tissue. Conclusions: The current study approach offers an overall look at molecular mechanisms that describe the cholesteatoma entity by focusing exclusively on the perimatrix processes in comparison to COM granulation tissue. The observed differences in gene expression between cholesteatoma perimatrix and COM granulation tissue could suggest novel markers potentially influenced by the perimatrix–matrix molecular interplay, which is not present in COM without cholesteatoma. Level of Evidence: NA. Laryngoscope, 130:E220–E227, 2020. © 2019 The American Laryngological, Rhinological and Otological Society, Inc.
T2  - The Laryngoscope
T1  - Perimatrix of middle ear cholesteatoma: A granulation tissue with a specific transcriptomic signature
VL  - 130
IS  - 4
SP  - E220
EP  - E227
DO  - 10.1002/lary.28084
ER  - 

@article{
author = "Jovanović, Ivan G. and Živković, Maja and Đurić, Tamara and Stojković, Ljiljana S. and Ješić, Snežana and Stanković, Aleksandra",
year = "2020",
abstract = "Objectives/Hypothesis: To establish comprehensive transcriptomic profiles of cholesteatoma perimatrix tissue and granulation tissue from chronic otitis media (COM) that did not develop cholesteatoma, which can indicate molecular pathways involved in the cholesteatoma perimatrix pathology and invasiveness. Study Design: Retrospective Case Series. Methods: Transcriptome data were obtained from cholesteatoma perimatrix tissue and COM granulation tissue by an Illumina iScan microarray. Differentially expressed genes (DEGs) were subsequently analyzed using both bioinformatical functional annotation and network analysis. Expression of candidate genes (MMP9 and LCN2) was validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) on a larger group of samples. Results: Analysis of the transcriptome led to the identification of 169 differentially expressed genes between investigated tissues. Bioinformatic analysis suggested that most significant biological processes involving DEGs were previously described in cholesteatoma pathology. Network analysis identified ERBB2, TFAP2A, and TP63 as major hubs of the DEGs molecular network. Furthermore, it was observed that the cellular component most significantly enriched in DEGs was extracellular space containing 47 DEGs. Using qRT-PCR, it was confirmed that mRNA levels of the major extracellular hub (MMP9) are increased, whereas its interacting molecule (LCN2) mRNA levels were decreased in cholesteatoma perimatrix tissue compared to COM granulation tissue. Conclusions: The current study approach offers an overall look at molecular mechanisms that describe the cholesteatoma entity by focusing exclusively on the perimatrix processes in comparison to COM granulation tissue. The observed differences in gene expression between cholesteatoma perimatrix and COM granulation tissue could suggest novel markers potentially influenced by the perimatrix–matrix molecular interplay, which is not present in COM without cholesteatoma. Level of Evidence: NA. Laryngoscope, 130:E220–E227, 2020. © 2019 The American Laryngological, Rhinological and Otological Society, Inc.",
journal = "The Laryngoscope",
title = "Perimatrix of middle ear cholesteatoma: A granulation tissue with a specific transcriptomic signature",
volume = "130",
number = "4",
pages = "E220-E227",
doi = "10.1002/lary.28084"
}

Jovanović, I. G., Živković, M., Đurić, T., Stojković, L. S., Ješić, S.,& Stanković, A.. (2020). Perimatrix of middle ear cholesteatoma: A granulation tissue with a specific transcriptomic signature. in The Laryngoscope, 130(4), E220-E227.
https://doi.org/10.1002/lary.28084

Jovanović IG, Živković M, Đurić T, Stojković LS, Ješić S, Stanković A. Perimatrix of middle ear cholesteatoma: A granulation tissue with a specific transcriptomic signature. in The Laryngoscope. 2020;130(4):E220-E227.
doi:10.1002/lary.28084 .

Jovanović, Ivan G., Živković, Maja, Đurić, Tamara, Stojković, Ljiljana S., Ješić, Snežana, Stanković, Aleksandra, "Perimatrix of middle ear cholesteatoma: A granulation tissue with a specific transcriptomic signature" in The Laryngoscope, 130, no. 4 (2020):E220-E227,
https://doi.org/10.1002/lary.28084 . .

TY  - JOUR
AU  - Kolić, Ivana
AU  - Stojković, Ljiljana S.
AU  - Dinčić, Evica
AU  - Jovanović, Ivan G.
AU  - Stanković, Aleksandra
AU  - Živković, Maja
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8618
AB  - Leptin (LEP) may contribute to the pathogenesis of multiple sclerosis (MS) by its immunomodulatory, proinflammatory and prooxidant effects. Therefore, plasma LEP levels and mRNA expression of five genes related to the LEP signaling pathway (LEP, LEP receptor (LEPR), peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC1A), superoxide dismutase 2, tumor necrosis factor-alpha) were investigated in relapsing-remitting MS. In patients (N = 64), compared to healthy subjects (N = 62), relative LEP mRNA levels were significantly increased (p = 0,01), while LEPR and PGC1A mRNA levels were decreased (p = 0,001 and p = 0,04, respectively). Significant positive correlation was observed between LEPR mRNA levels and clinical parameters of MS progression (EDSS, MSSS). © 2019
T2  - Journal of Neuroimmunology
T1  - Expression of LEP, LEPR and PGC1A genes is altered in peripheral blood mononuclear cells of patients with relapsing-remitting multiple sclerosis
VL  - 338
SP  - 577090
DO  - 10.1016/j.jneuroim.2019.577090
ER  - 

@article{
author = "Kolić, Ivana and Stojković, Ljiljana S. and Dinčić, Evica and Jovanović, Ivan G. and Stanković, Aleksandra and Živković, Maja",
year = "2020",
abstract = "Leptin (LEP) may contribute to the pathogenesis of multiple sclerosis (MS) by its immunomodulatory, proinflammatory and prooxidant effects. Therefore, plasma LEP levels and mRNA expression of five genes related to the LEP signaling pathway (LEP, LEP receptor (LEPR), peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC1A), superoxide dismutase 2, tumor necrosis factor-alpha) were investigated in relapsing-remitting MS. In patients (N = 64), compared to healthy subjects (N = 62), relative LEP mRNA levels were significantly increased (p = 0,01), while LEPR and PGC1A mRNA levels were decreased (p = 0,001 and p = 0,04, respectively). Significant positive correlation was observed between LEPR mRNA levels and clinical parameters of MS progression (EDSS, MSSS). © 2019",
journal = "Journal of Neuroimmunology",
title = "Expression of LEP, LEPR and PGC1A genes is altered in peripheral blood mononuclear cells of patients with relapsing-remitting multiple sclerosis",
volume = "338",
pages = "577090",
doi = "10.1016/j.jneuroim.2019.577090"
}

Kolić, I., Stojković, L. S., Dinčić, E., Jovanović, I. G., Stanković, A.,& Živković, M.. (2020). Expression of LEP, LEPR and PGC1A genes is altered in peripheral blood mononuclear cells of patients with relapsing-remitting multiple sclerosis. in Journal of Neuroimmunology, 338, 577090.
https://doi.org/10.1016/j.jneuroim.2019.577090

Kolić I, Stojković LS, Dinčić E, Jovanović IG, Stanković A, Živković M. Expression of LEP, LEPR and PGC1A genes is altered in peripheral blood mononuclear cells of patients with relapsing-remitting multiple sclerosis. in Journal of Neuroimmunology. 2020;338:577090.
doi:10.1016/j.jneuroim.2019.577090 .

Kolić, Ivana, Stojković, Ljiljana S., Dinčić, Evica, Jovanović, Ivan G., Stanković, Aleksandra, Živković, Maja, "Expression of LEP, LEPR and PGC1A genes is altered in peripheral blood mononuclear cells of patients with relapsing-remitting multiple sclerosis" in Journal of Neuroimmunology, 338 (2020):577090,
https://doi.org/10.1016/j.jneuroim.2019.577090 . .

TY  - CHAP
AU  - Stanković, Aleksandra
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8682
AB  - During the last decade, quantitative measurement of the methylation status in white blood cells (WBCs) has been used as a potential biomarker in a variety of diseases. Long interspersed nucleotide element-1 (LINE-1) has been used widely as a surrogate marker of global DNA methylation. Altered maternal DNA methylation is suggested to be an underlying mechanism in the trisomy 21 and the development of birth defects, including congenital heart defects (CHDs). The molecular mechanisms that underlie the epigenetic regulation of gene transcription are independent of DNA sequence, but they do depend on environmental stimuli, which are especially important in fetal development in utero environment. Folic acid deficiency and genetic variations of folate pathway genes, such as the methylenetetrahydrofolate reductase gene (MTHFR), are foremost among these maternal risk factors. Also, there are exogenous risk factors (cigarette smoking, alcohol intake, medication use, periconceptional maternal supplementation, body mass index, and dietary habits) with impact on maternal LINE-1 methylation. MTHFR C677T genotype/diet and other environmental factors as significant predictors of LINE-1 DNA methylation in regard to congenital diseases will be discussed in the chapter.
PB  - IntechOpen
T2  - DNA Methylation Mechanism
T1  - Global DNA Methylation as a Potential Underlying Mechanism of Congenital Disease Development
VL  - Ch. 3
SP  - 1
EP  - 21
DO  - 10.5772/intechopen.90996
ER  - 

@inbook{
author = "Stanković, Aleksandra",
year = "2020",
abstract = "During the last decade, quantitative measurement of the methylation status in white blood cells (WBCs) has been used as a potential biomarker in a variety of diseases. Long interspersed nucleotide element-1 (LINE-1) has been used widely as a surrogate marker of global DNA methylation. Altered maternal DNA methylation is suggested to be an underlying mechanism in the trisomy 21 and the development of birth defects, including congenital heart defects (CHDs). The molecular mechanisms that underlie the epigenetic regulation of gene transcription are independent of DNA sequence, but they do depend on environmental stimuli, which are especially important in fetal development in utero environment. Folic acid deficiency and genetic variations of folate pathway genes, such as the methylenetetrahydrofolate reductase gene (MTHFR), are foremost among these maternal risk factors. Also, there are exogenous risk factors (cigarette smoking, alcohol intake, medication use, periconceptional maternal supplementation, body mass index, and dietary habits) with impact on maternal LINE-1 methylation. MTHFR C677T genotype/diet and other environmental factors as significant predictors of LINE-1 DNA methylation in regard to congenital diseases will be discussed in the chapter.",
publisher = "IntechOpen",
journal = "DNA Methylation Mechanism",
booktitle = "Global DNA Methylation as a Potential Underlying Mechanism of Congenital Disease Development",
volume = "Ch. 3",
pages = "1-21",
doi = "10.5772/intechopen.90996"
}

Stanković, A.. (2020). Global DNA Methylation as a Potential Underlying Mechanism of Congenital Disease Development. in DNA Methylation Mechanism
IntechOpen., Ch. 3, 1-21.
https://doi.org/10.5772/intechopen.90996

Stanković A. Global DNA Methylation as a Potential Underlying Mechanism of Congenital Disease Development. in DNA Methylation Mechanism. 2020;Ch. 3:1-21.
doi:10.5772/intechopen.90996 .

Stanković, Aleksandra, "Global DNA Methylation as a Potential Underlying Mechanism of Congenital Disease Development" in DNA Methylation Mechanism, Ch. 3 (2020):1-21,
https://doi.org/10.5772/intechopen.90996 . .

TY  - JOUR
AU  - Životić, Ivan
AU  - Đurić, Tamara
AU  - Stanković, Aleksandra
AU  - Milašinović, Dejan
AU  - Stanković, Goran
AU  - Dekleva, Milica
AU  - Marković-Nikolić, Nataša
AU  - Alavantić, Dragan
AU  - Živković, Maja
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8432
AB  - Background: Chromosomal region 9p21.3 is most robustly associated with coronary artery disease (CAD) in western European populations. However, heterogeneity in CAD phenotypes leads to uncertainty whether 9p21.3 is associated with stable and/or acute clinical presentations of CAD. 9p21.3 is rich in regulatory elements, but the underlying mechanisms of its actions in CAD remain unclear. We investigate the association of 9p21.3 two haplotype blocks lead variants (rs10757278 and rs518394) with first-ever non-fatal myocardial infarction (MI) in CAD patients and their association with CDKN2B mRNA expression in peripheral blood mononuclear cells 6 months after the event. Methods: We included CAD patients with sustained first MI (n = 523) and controls (n = 583). Gene expression was assessed in 72 patients 6 months after MI and 43 healthy controls. TaqMan® technology was used for the gene expression and genotyping analysis. Results: CDKN2B mRNA was significantly lower in MI patients compared with the controls (p = 0.002) and in patients carrying the rs10757278 G risk allele versus AA homozygotes (p = 0.012) 6 months after the event. While we confirmed the association of rs10757278 with CDKN2B expression in MI patients, we failed to find an association between the investigated variants and MI or disease burden. Conclusions: We suggest a dysregulation of gene expression in the 9p21.3 region six months after acute MI, which is affected by a genetic variant in patients. The rs10757278 rare allele is one factor that might lead to prolonged risk for proatherogenic complications. © 2019 The Canadian Society of Clinical Chemists
T2  - Clinical Biochemistry
T1  - CDKN2B gene expression is affected by 9p21.3 rs10757278 in CAD patients, six months after the MI
VL  - 73
SP  - 70
EP  - 76
DO  - 10.1016/j.clinbiochem.2019.08.003
ER  - 

@article{
author = "Životić, Ivan and Đurić, Tamara and Stanković, Aleksandra and Milašinović, Dejan and Stanković, Goran and Dekleva, Milica and Marković-Nikolić, Nataša and Alavantić, Dragan and Živković, Maja",
year = "2019",
abstract = "Background: Chromosomal region 9p21.3 is most robustly associated with coronary artery disease (CAD) in western European populations. However, heterogeneity in CAD phenotypes leads to uncertainty whether 9p21.3 is associated with stable and/or acute clinical presentations of CAD. 9p21.3 is rich in regulatory elements, but the underlying mechanisms of its actions in CAD remain unclear. We investigate the association of 9p21.3 two haplotype blocks lead variants (rs10757278 and rs518394) with first-ever non-fatal myocardial infarction (MI) in CAD patients and their association with CDKN2B mRNA expression in peripheral blood mononuclear cells 6 months after the event. Methods: We included CAD patients with sustained first MI (n = 523) and controls (n = 583). Gene expression was assessed in 72 patients 6 months after MI and 43 healthy controls. TaqMan® technology was used for the gene expression and genotyping analysis. Results: CDKN2B mRNA was significantly lower in MI patients compared with the controls (p = 0.002) and in patients carrying the rs10757278 G risk allele versus AA homozygotes (p = 0.012) 6 months after the event. While we confirmed the association of rs10757278 with CDKN2B expression in MI patients, we failed to find an association between the investigated variants and MI or disease burden. Conclusions: We suggest a dysregulation of gene expression in the 9p21.3 region six months after acute MI, which is affected by a genetic variant in patients. The rs10757278 rare allele is one factor that might lead to prolonged risk for proatherogenic complications. © 2019 The Canadian Society of Clinical Chemists",
journal = "Clinical Biochemistry",
title = "CDKN2B gene expression is affected by 9p21.3 rs10757278 in CAD patients, six months after the MI",
volume = "73",
pages = "70-76",
doi = "10.1016/j.clinbiochem.2019.08.003"
}

Životić, I., Đurić, T., Stanković, A., Milašinović, D., Stanković, G., Dekleva, M., Marković-Nikolić, N., Alavantić, D.,& Živković, M.. (2019). CDKN2B gene expression is affected by 9p21.3 rs10757278 in CAD patients, six months after the MI. in Clinical Biochemistry, 73, 70-76.
https://doi.org/10.1016/j.clinbiochem.2019.08.003

Životić I, Đurić T, Stanković A, Milašinović D, Stanković G, Dekleva M, Marković-Nikolić N, Alavantić D, Živković M. CDKN2B gene expression is affected by 9p21.3 rs10757278 in CAD patients, six months after the MI. in Clinical Biochemistry. 2019;73:70-76.
doi:10.1016/j.clinbiochem.2019.08.003 .

Životić, Ivan, Đurić, Tamara, Stanković, Aleksandra, Milašinović, Dejan, Stanković, Goran, Dekleva, Milica, Marković-Nikolić, Nataša, Alavantić, Dragan, Živković, Maja, "CDKN2B gene expression is affected by 9p21.3 rs10757278 in CAD patients, six months after the MI" in Clinical Biochemistry, 73 (2019):70-76,
https://doi.org/10.1016/j.clinbiochem.2019.08.003 . .

TY  - JOUR
AU  - Bošković, Maja
AU  - Bundalo, Maja M.
AU  - Živković, Maja
AU  - Stanišić, Jelena
AU  - Kostić, Milan
AU  - Korićanac, Goran
AU  - Stanković, Aleksandra
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7984
AB  - Harmful effects of fructose-rich diet (FRD) were predominantly observed in males, suggesting protective effects of estrogens. Little is known about AMPK/sirtuin-1 (SIRT1)/forkhead box O3 (FoxO3a)/manganese superoxide dismutase (MnSOD)/catalase signaling in the heart in state of metabolic syndrome and oxidative stress induced by fructose over-consumption. We investigated the effect of 10% FRD on expression of AMPK-SIRT1-FoxO3a-MnSOD/catalase axis in myocardium and potentially beneficial effect of 17β-estradiol replacement. The expression of NADPH oxidase 4 (Nox4) and miRNA-155, unfavorable regulators of this axis, were also investigated. FRD significantly increased AMPK and decreased FoxO3a activity, decreased SIRT1, MnSOD and Nox4 protein expression while E2 reverted these changes, except for Nox4, and increased catalase protein level. E2 diminished Nox4 and MnSOD mRNA level in FRD ovariectomized rats. These results suggest independent response of AMPK and SIRT to FRD treatment. The proposed signaling in the heart should be further investigated in the prooxidative and antioxidative milieu.
T2  - Journal of Functional Foods
T1  - Estradiol ameliorates antioxidant axis SIRT1-FoxO3a-MnSOD/catalase in the heart of fructose-fed ovariectomized rats
VL  - 52
SP  - 690
EP  - 698
DO  - 10.1016/j.jff.2018.11.053
ER  - 

@article{
author = "Bošković, Maja and Bundalo, Maja M. and Živković, Maja and Stanišić, Jelena and Kostić, Milan and Korićanac, Goran and Stanković, Aleksandra",
year = "2019",
abstract = "Harmful effects of fructose-rich diet (FRD) were predominantly observed in males, suggesting protective effects of estrogens. Little is known about AMPK/sirtuin-1 (SIRT1)/forkhead box O3 (FoxO3a)/manganese superoxide dismutase (MnSOD)/catalase signaling in the heart in state of metabolic syndrome and oxidative stress induced by fructose over-consumption. We investigated the effect of 10% FRD on expression of AMPK-SIRT1-FoxO3a-MnSOD/catalase axis in myocardium and potentially beneficial effect of 17β-estradiol replacement. The expression of NADPH oxidase 4 (Nox4) and miRNA-155, unfavorable regulators of this axis, were also investigated. FRD significantly increased AMPK and decreased FoxO3a activity, decreased SIRT1, MnSOD and Nox4 protein expression while E2 reverted these changes, except for Nox4, and increased catalase protein level. E2 diminished Nox4 and MnSOD mRNA level in FRD ovariectomized rats. These results suggest independent response of AMPK and SIRT to FRD treatment. The proposed signaling in the heart should be further investigated in the prooxidative and antioxidative milieu.",
journal = "Journal of Functional Foods",
title = "Estradiol ameliorates antioxidant axis SIRT1-FoxO3a-MnSOD/catalase in the heart of fructose-fed ovariectomized rats",
volume = "52",
pages = "690-698",
doi = "10.1016/j.jff.2018.11.053"
}

Bošković, M., Bundalo, M. M., Živković, M., Stanišić, J., Kostić, M., Korićanac, G.,& Stanković, A.. (2019). Estradiol ameliorates antioxidant axis SIRT1-FoxO3a-MnSOD/catalase in the heart of fructose-fed ovariectomized rats. in Journal of Functional Foods, 52, 690-698.
https://doi.org/10.1016/j.jff.2018.11.053

Bošković M, Bundalo MM, Živković M, Stanišić J, Kostić M, Korićanac G, Stanković A. Estradiol ameliorates antioxidant axis SIRT1-FoxO3a-MnSOD/catalase in the heart of fructose-fed ovariectomized rats. in Journal of Functional Foods. 2019;52:690-698.
doi:10.1016/j.jff.2018.11.053 .

Bošković, Maja, Bundalo, Maja M., Živković, Maja, Stanišić, Jelena, Kostić, Milan, Korićanac, Goran, Stanković, Aleksandra, "Estradiol ameliorates antioxidant axis SIRT1-FoxO3a-MnSOD/catalase in the heart of fructose-fed ovariectomized rats" in Journal of Functional Foods, 52 (2019):690-698,
https://doi.org/10.1016/j.jff.2018.11.053 . .

TY  - JOUR
AU  - Životić, Ivan
AU  - Đurić, Tamara
AU  - Stanković, Aleksandra
AU  - Ivancevic, Ilija
AU  - Končar, Igor
AU  - Milašinović, Dejan
AU  - Stanković, Goran
AU  - Alavantić, Dragan
AU  - Živković, Maja
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1843
AB  - The 9p21.3 region is rich in regulatory elements and the variants in this region had been robustly associated with carotid plaque (CP) and coronary artery disease (CAD). Recently, the HACD4 was detected as one of the six 9p21.3 differentially expressed genes associated with accelerated atherosclerosis and greater mean lesion area in the Athsq1 congenic mice. We aimed to investigate association of two potentially regulatory HACD4 variants (rs36212560 I/D, rs2275888 T/C) and their haplotypes with CP occurrence and the level of HACD4 and FOCAD mRNA in human CP tissue. Association study was replicated in CAD patients who suffered the first myocardial infarction. Study included 477 CP patients, 303 healthy controls and replication sample of 224 CAD males from the population of Serbia. Genotypes were determined by polymerase chain reaction (PCR) and real-time PCR using TaqMan (R) technology. The gene expression was detected with TaqMan (R) technology. We have found significant and independent association of DT haplotype with CP presence in men (adjusted OR = 1.64 CI = 1.12-2.42, p = 0.011). The result was replicated in CAD males (adjusted OR = 1.84 CI = 1.21-2.80, p = 0.004). We have found significant effect of the HACD4 rs2275888 on FOCAD mRNA level in human CP tissue. Correction for multiple testing was performed. Independent association of HACD4 haplotypes with atherosclerotic phenotypes connotes a further validation and replication in larger cohorts as well as functional studies to enlighten the potential mechanism of its action in pathophysiology of atherosclerosis.
T2  - Gene
T1  - The HACD4 haplotype as a risk factor for atherosclerosis in males
VL  - 641
SP  - 35
EP  - 40
DO  - 10.1016/j.gene.2017.10.030
ER  - 

@article{
author = "Životić, Ivan and Đurić, Tamara and Stanković, Aleksandra and Ivancevic, Ilija and Končar, Igor and Milašinović, Dejan and Stanković, Goran and Alavantić, Dragan and Živković, Maja",
year = "2018",
abstract = "The 9p21.3 region is rich in regulatory elements and the variants in this region had been robustly associated with carotid plaque (CP) and coronary artery disease (CAD). Recently, the HACD4 was detected as one of the six 9p21.3 differentially expressed genes associated with accelerated atherosclerosis and greater mean lesion area in the Athsq1 congenic mice. We aimed to investigate association of two potentially regulatory HACD4 variants (rs36212560 I/D, rs2275888 T/C) and their haplotypes with CP occurrence and the level of HACD4 and FOCAD mRNA in human CP tissue. Association study was replicated in CAD patients who suffered the first myocardial infarction. Study included 477 CP patients, 303 healthy controls and replication sample of 224 CAD males from the population of Serbia. Genotypes were determined by polymerase chain reaction (PCR) and real-time PCR using TaqMan (R) technology. The gene expression was detected with TaqMan (R) technology. We have found significant and independent association of DT haplotype with CP presence in men (adjusted OR = 1.64 CI = 1.12-2.42, p = 0.011). The result was replicated in CAD males (adjusted OR = 1.84 CI = 1.21-2.80, p = 0.004). We have found significant effect of the HACD4 rs2275888 on FOCAD mRNA level in human CP tissue. Correction for multiple testing was performed. Independent association of HACD4 haplotypes with atherosclerotic phenotypes connotes a further validation and replication in larger cohorts as well as functional studies to enlighten the potential mechanism of its action in pathophysiology of atherosclerosis.",
journal = "Gene",
title = "The HACD4 haplotype as a risk factor for atherosclerosis in males",
volume = "641",
pages = "35-40",
doi = "10.1016/j.gene.2017.10.030"
}

Životić, I., Đurić, T., Stanković, A., Ivancevic, I., Končar, I., Milašinović, D., Stanković, G., Alavantić, D.,& Živković, M.. (2018). The HACD4 haplotype as a risk factor for atherosclerosis in males. in Gene, 641, 35-40.
https://doi.org/10.1016/j.gene.2017.10.030

Životić I, Đurić T, Stanković A, Ivancevic I, Končar I, Milašinović D, Stanković G, Alavantić D, Živković M. The HACD4 haplotype as a risk factor for atherosclerosis in males. in Gene. 2018;641:35-40.
doi:10.1016/j.gene.2017.10.030 .

Životić, Ivan, Đurić, Tamara, Stanković, Aleksandra, Ivancevic, Ilija, Končar, Igor, Milašinović, Dejan, Stanković, Goran, Alavantić, Dragan, Živković, Maja, "The HACD4 haplotype as a risk factor for atherosclerosis in males" in Gene, 641 (2018):35-40,
https://doi.org/10.1016/j.gene.2017.10.030 . .

TY  - JOUR
AU  - Jovanović, Ivan G.
AU  - Živković, Maja
AU  - Kostić, Mirjana M.
AU  - Krstić, Zoran
AU  - Đurić, Tamara
AU  - Licastro, Danilo
AU  - Meroni, Germana
AU  - Alavantić, Dragan
AU  - Stanković, Aleksandra
PY  - 2018
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0024320518305940
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7891
AB  - Aims: (1) to identify the most dysregulated genes in ureter tissue affected by congenital anomalies of the kidney and urinary tract (CAKUT) and to extract the biological meaning of these markers; (2) to describe the key molecular networks in CAKUT and to provide expression validation of the genes selected from these networks. Main methods: Transcriptome data was obtained from ureter samples of CAKUT patients and controls by Illumina iScan microarray. Identification of differentially expressed genes was coupled with subsequent bioinformatics analyses. Expression of candidate genes was validated by qRT-PCR. Key findings: Analysis of the transcriptome led to the identification of 78 commonly dysregulated genes in CAKUT tissue compared to controls. Integrative bioinformatic analyses of differentially expressed genes identified 7 major networks. The targets for qRT-PCR validation were selected as members of the major molecular networks in CAKUT, which had both, the significant high fold change and biological relevance for CAKUT. By qRT-PCR the substantial increase of LCN2, PROM1, SOSTDC1, and decrease of INA, RASD1 and TAC3 mRNA levels was confirmed. Significance: Since CAKUT is a leading cause of end-stage renal disease in children, the search for molecular targets for postnatal therapy is of particular interest. Data described in this study represents the gene expression profile and significant molecular networks specific to human ureter affected by CAKUT. The discovery of impaired molecular factors and processes is the step towards the uncovering of the key mechanisms that reflect CAKUT postnatally and could lead to the affected tissue deterioration and end organ damage. © 2018 Elsevier Inc.
T2  - Life Sciences
T1  - Transcriptome-driven integrative exploration of functional state of ureter tissue affected by CAKUT
VL  - 212
SP  - 1
EP  - 8
DO  - 10.1016/j.lfs.2018.09.042
ER  - 

@article{
author = "Jovanović, Ivan G. and Živković, Maja and Kostić, Mirjana M. and Krstić, Zoran and Đurić, Tamara and Licastro, Danilo and Meroni, Germana and Alavantić, Dragan and Stanković, Aleksandra",
year = "2018",
abstract = "Aims: (1) to identify the most dysregulated genes in ureter tissue affected by congenital anomalies of the kidney and urinary tract (CAKUT) and to extract the biological meaning of these markers; (2) to describe the key molecular networks in CAKUT and to provide expression validation of the genes selected from these networks. Main methods: Transcriptome data was obtained from ureter samples of CAKUT patients and controls by Illumina iScan microarray. Identification of differentially expressed genes was coupled with subsequent bioinformatics analyses. Expression of candidate genes was validated by qRT-PCR. Key findings: Analysis of the transcriptome led to the identification of 78 commonly dysregulated genes in CAKUT tissue compared to controls. Integrative bioinformatic analyses of differentially expressed genes identified 7 major networks. The targets for qRT-PCR validation were selected as members of the major molecular networks in CAKUT, which had both, the significant high fold change and biological relevance for CAKUT. By qRT-PCR the substantial increase of LCN2, PROM1, SOSTDC1, and decrease of INA, RASD1 and TAC3 mRNA levels was confirmed. Significance: Since CAKUT is a leading cause of end-stage renal disease in children, the search for molecular targets for postnatal therapy is of particular interest. Data described in this study represents the gene expression profile and significant molecular networks specific to human ureter affected by CAKUT. The discovery of impaired molecular factors and processes is the step towards the uncovering of the key mechanisms that reflect CAKUT postnatally and could lead to the affected tissue deterioration and end organ damage. © 2018 Elsevier Inc.",
journal = "Life Sciences",
title = "Transcriptome-driven integrative exploration of functional state of ureter tissue affected by CAKUT",
volume = "212",
pages = "1-8",
doi = "10.1016/j.lfs.2018.09.042"
}

Jovanović, I. G., Živković, M., Kostić, M. M., Krstić, Z., Đurić, T., Licastro, D., Meroni, G., Alavantić, D.,& Stanković, A.. (2018). Transcriptome-driven integrative exploration of functional state of ureter tissue affected by CAKUT. in Life Sciences, 212, 1-8.
https://doi.org/10.1016/j.lfs.2018.09.042

Jovanović IG, Živković M, Kostić MM, Krstić Z, Đurić T, Licastro D, Meroni G, Alavantić D, Stanković A. Transcriptome-driven integrative exploration of functional state of ureter tissue affected by CAKUT. in Life Sciences. 2018;212:1-8.
doi:10.1016/j.lfs.2018.09.042 .

Jovanović, Ivan G., Živković, Maja, Kostić, Mirjana M., Krstić, Zoran, Đurić, Tamara, Licastro, Danilo, Meroni, Germana, Alavantić, Dragan, Stanković, Aleksandra, "Transcriptome-driven integrative exploration of functional state of ureter tissue affected by CAKUT" in Life Sciences, 212 (2018):1-8,
https://doi.org/10.1016/j.lfs.2018.09.042 . .

TY  - JOUR
AU  - Željić, Katarina
AU  - Jovanović, Ivan G.
AU  - Jovanović, Jasmina
AU  - Magić, Zvonko
AU  - Stanković, Aleksandra
AU  - Šupić, Gordana
PY  - 2018
UR  - https://www.tandfonline.com/doi/full/10.1080/03009734.2018.1439551
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7630
AB  - Aim: It was the aim of the study to identify commonly deregulated miRNAs in oral cancer patients by performing a meta-analysis of previously published miRNA expression profiles in cancer and matched normal non-cancerous tissue in such patients. Material and methods: Meta-analysis included seven independent studies analyzed by a vote-counting method followed by bioinformatic enrichment analysis. Results: Amongst seven independent studies included in the meta-analysis, 20 miRNAs were found to be deregulated in oral cancer when compared with non-cancerous tissue. Eleven miRNAs were consistently up-regulated in three or more studies (miR-21-5p, miR-31-5p, miR-135b-5p, miR-31-3p, miR-93-5p, miR-34b-5p, miR-424-5p, miR-18a-5p, miR-455-3p, miR-450a-5p, miR-21-3p), and nine were down-regulated (miR-139-5p, miR-30a-3p, miR-376c-3p, miR-885-5p, miR-375, miR-486-5p, miR-411-5p, miR-133a-3p, miR-30a-5p). The meta-signature of identified miRNAs was functionally characterized by KEGG enrichment analysis. Twenty-four KEGG pathways were significantly enriched, and TGF-beta signaling was the most enriched signaling pathway. The highest number of meta-signature miRNAs was involved in the sphingolipid signaling pathway. Natural killer cell-mediated cytotoxicity was the pathway with most genes regulated by identified miRNAs. The rest of the enriched pathways in our miRNA list describe different malignancies and signaling. Conclusions: The identified miRNA meta-signature might be considered as a potential battery of biomarkers when distinguishing oral cancer tissue from normal, non-cancerous tissue. Further mechanistic studies are warranted in order to confirm and fully elucidate the role of deregulated miRNAs in oral cancer.
T2  - Upsala Journal of Medical Sciences
T1  - MicroRNA meta-signature of oral cancer: evidence from a meta-analysis
VL  - 123
IS  - 1
SP  - 43
EP  - 49
DO  - 10.1080/03009734.2018.1439551
ER  - 

@article{
author = "Željić, Katarina and Jovanović, Ivan G. and Jovanović, Jasmina and Magić, Zvonko and Stanković, Aleksandra and Šupić, Gordana",
year = "2018",
abstract = "Aim: It was the aim of the study to identify commonly deregulated miRNAs in oral cancer patients by performing a meta-analysis of previously published miRNA expression profiles in cancer and matched normal non-cancerous tissue in such patients. Material and methods: Meta-analysis included seven independent studies analyzed by a vote-counting method followed by bioinformatic enrichment analysis. Results: Amongst seven independent studies included in the meta-analysis, 20 miRNAs were found to be deregulated in oral cancer when compared with non-cancerous tissue. Eleven miRNAs were consistently up-regulated in three or more studies (miR-21-5p, miR-31-5p, miR-135b-5p, miR-31-3p, miR-93-5p, miR-34b-5p, miR-424-5p, miR-18a-5p, miR-455-3p, miR-450a-5p, miR-21-3p), and nine were down-regulated (miR-139-5p, miR-30a-3p, miR-376c-3p, miR-885-5p, miR-375, miR-486-5p, miR-411-5p, miR-133a-3p, miR-30a-5p). The meta-signature of identified miRNAs was functionally characterized by KEGG enrichment analysis. Twenty-four KEGG pathways were significantly enriched, and TGF-beta signaling was the most enriched signaling pathway. The highest number of meta-signature miRNAs was involved in the sphingolipid signaling pathway. Natural killer cell-mediated cytotoxicity was the pathway with most genes regulated by identified miRNAs. The rest of the enriched pathways in our miRNA list describe different malignancies and signaling. Conclusions: The identified miRNA meta-signature might be considered as a potential battery of biomarkers when distinguishing oral cancer tissue from normal, non-cancerous tissue. Further mechanistic studies are warranted in order to confirm and fully elucidate the role of deregulated miRNAs in oral cancer.",
journal = "Upsala Journal of Medical Sciences",
title = "MicroRNA meta-signature of oral cancer: evidence from a meta-analysis",
volume = "123",
number = "1",
pages = "43-49",
doi = "10.1080/03009734.2018.1439551"
}

Željić, K., Jovanović, I. G., Jovanović, J., Magić, Z., Stanković, A.,& Šupić, G.. (2018). MicroRNA meta-signature of oral cancer: evidence from a meta-analysis. in Upsala Journal of Medical Sciences, 123(1), 43-49.
https://doi.org/10.1080/03009734.2018.1439551

Željić K, Jovanović IG, Jovanović J, Magić Z, Stanković A, Šupić G. MicroRNA meta-signature of oral cancer: evidence from a meta-analysis. in Upsala Journal of Medical Sciences. 2018;123(1):43-49.
doi:10.1080/03009734.2018.1439551 .

Željić, Katarina, Jovanović, Ivan G., Jovanović, Jasmina, Magić, Zvonko, Stanković, Aleksandra, Šupić, Gordana, "MicroRNA meta-signature of oral cancer: evidence from a meta-analysis" in Upsala Journal of Medical Sciences, 123, no. 1 (2018):43-49,
https://doi.org/10.1080/03009734.2018.1439551 . .

TY  - DATA
AU  - Željić, Katarina
AU  - Jovanović, Ivan G.
AU  - Jovanović, Jasmina
AU  - Magić, Zvonko
AU  - Stanković, Aleksandra
AU  - Šupić, Gordana
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7843
AB  - Aim: It was the aim of the study to identify commonly deregulated miRNAs in oral cancer patients by performing a meta-analysis of previously published miRNA expression profiles in cancer and matched normal non-cancerous tissue in such patients. Material and methods: Meta-analysis included seven independent studies analyzed by a vote-counting method followed by bioinformatic enrichment analysis. Results: Amongst seven independent studies included in the meta-analysis, 20 miRNAs were found to be deregulated in oral cancer when compared with non-cancerous tissue. Eleven miRNAs were consistently up-regulated in three or more studies (miR-21-5p, miR-31-5p, miR-135b-5p, miR-31-3p, miR-93-5p, miR-34b-5p, miR-424-5p, miR-18a-5p, miR-455-3p, miR-450a-5p, miR-21-3p), and nine were down-regulated (miR-139-5p, miR-30a-3p, miR-376c-3p, miR-885-5p, miR-375, miR-486-5p, miR-411-5p, miR-133a-3p, miR-30a-5p). The meta-signature of identified miRNAs was functionally characterized by KEGG enrichment analysis. Twenty-four KEGG pathways were significantly enriched, and TGF-beta signaling was the most enriched signaling pathway. The highest number of meta-signature miRNAs was involved in the sphingolipid signaling pathway. Natural killer cell-mediated cytotoxicity was the pathway with most genes regulated by identified miRNAs. The rest of the enriched pathways in our miRNA list describe different malignancies and signaling. Conclusions: The identified miRNA meta-signature might be considered as a potential battery of biomarkers when distinguishing oral cancer tissue from normal, non-cancerous tissue. Further mechanistic studies are warranted in order to confirm and fully elucidate the role of deregulated miRNAs in oral cancer.
T2  - Upsala Journal of Medical Sciences
T1  - MicroRNA meta-signature of oral cancer: evidence from a meta-analysis
VL  - 123
IS  - 1
SP  - 43
EP  - 49
DO  - 10.6084/m9.figshare.5926675
ER  - 

@misc{
author = "Željić, Katarina and Jovanović, Ivan G. and Jovanović, Jasmina and Magić, Zvonko and Stanković, Aleksandra and Šupić, Gordana",
year = "2018",
abstract = "Aim: It was the aim of the study to identify commonly deregulated miRNAs in oral cancer patients by performing a meta-analysis of previously published miRNA expression profiles in cancer and matched normal non-cancerous tissue in such patients. Material and methods: Meta-analysis included seven independent studies analyzed by a vote-counting method followed by bioinformatic enrichment analysis. Results: Amongst seven independent studies included in the meta-analysis, 20 miRNAs were found to be deregulated in oral cancer when compared with non-cancerous tissue. Eleven miRNAs were consistently up-regulated in three or more studies (miR-21-5p, miR-31-5p, miR-135b-5p, miR-31-3p, miR-93-5p, miR-34b-5p, miR-424-5p, miR-18a-5p, miR-455-3p, miR-450a-5p, miR-21-3p), and nine were down-regulated (miR-139-5p, miR-30a-3p, miR-376c-3p, miR-885-5p, miR-375, miR-486-5p, miR-411-5p, miR-133a-3p, miR-30a-5p). The meta-signature of identified miRNAs was functionally characterized by KEGG enrichment analysis. Twenty-four KEGG pathways were significantly enriched, and TGF-beta signaling was the most enriched signaling pathway. The highest number of meta-signature miRNAs was involved in the sphingolipid signaling pathway. Natural killer cell-mediated cytotoxicity was the pathway with most genes regulated by identified miRNAs. The rest of the enriched pathways in our miRNA list describe different malignancies and signaling. Conclusions: The identified miRNA meta-signature might be considered as a potential battery of biomarkers when distinguishing oral cancer tissue from normal, non-cancerous tissue. Further mechanistic studies are warranted in order to confirm and fully elucidate the role of deregulated miRNAs in oral cancer.",
journal = "Upsala Journal of Medical Sciences",
title = "MicroRNA meta-signature of oral cancer: evidence from a meta-analysis",
volume = "123",
number = "1",
pages = "43-49",
doi = "10.6084/m9.figshare.5926675"
}

Željić, K., Jovanović, I. G., Jovanović, J., Magić, Z., Stanković, A.,& Šupić, G.. (2018). MicroRNA meta-signature of oral cancer: evidence from a meta-analysis. in Upsala Journal of Medical Sciences, 123(1), 43-49.
https://doi.org/10.6084/m9.figshare.5926675

Željić K, Jovanović IG, Jovanović J, Magić Z, Stanković A, Šupić G. MicroRNA meta-signature of oral cancer: evidence from a meta-analysis. in Upsala Journal of Medical Sciences. 2018;123(1):43-49.
doi:10.6084/m9.figshare.5926675 .

Željić, Katarina, Jovanović, Ivan G., Jovanović, Jasmina, Magić, Zvonko, Stanković, Aleksandra, Šupić, Gordana, "MicroRNA meta-signature of oral cancer: evidence from a meta-analysis" in Upsala Journal of Medical Sciences, 123, no. 1 (2018):43-49,
https://doi.org/10.6084/m9.figshare.5926675 . .

TY  - JOUR
AU  - Živković, Maja
AU  - Kolić, Ivana
AU  - Ješić, Snežana
AU  - Jotić, Ana
AU  - Stanković, Aleksandra
PY  - 2018
UR  - http://e-ceo.org/journal/view.php?doi=10.21053/ceo.2017.01060
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7677
AB  - Objectives. Chronic otitis media (COM) is followed by irreversible tissue damage and destruction of the middle ear structures, with the possibility of complications under the maintenance of inflammation. Inflammatory mediators such as cytokines play a crucial role in the initial stage of inflammation. The aim of this study was to evaluate the association of the polymorphisms in two innate immunity/inflammation cascade genes from interleukin-1 (IL-1) gene cluster with COM with regard to cholesteatoma. Methods. In the cross-sectional case-control study, DNA samples were collected from 189 patients with COM and 119 controls from a population of Serbia. The +3953 C/T (rs1143634), TaqI polymorphism in interleukin-1 beta (IL-1Β) gene and 86 bp variable number tandem repeat (VNTR, rs2234663) polymorphism in the IL-1 receptor antagonist (IL-1RA) gene were analyzed by polymerase chain reaction. Results. The IL-1Β TaqI polymorphism was not significantly different in patients compared with the control group. The significant difference between patients and controls was observed for both, genotype and allele frequencies of IL-1RA VNTR polymorphism (chi-square P<0.01). We found that carriers of IL-1RA allele 2 (odds ratio, 0.47; 95% confidence interval, 0.29 to 0.76; P=0.004) have a favorable association with COM, using multivariate logistic analysis that included both polymorphisms, age and sex. The IL-1RA allele frequency distribution was significantly different with regard to cholesteatoma. Conclusion. The carriers of allele 2 of VNTR IL-1RA polymorphism had a decreased odds ratio for COM, which is in agreement with findings in other inflammatory disease and its previous association with higher IL-1RA levels. Possible down-regulation of IL-1 mediated proinflammatory signaling pathways via IL-1RA in COM as well as results of our study should be further investigated and replicated.
T2  - Clinical and Experimental Otorhinolaryngology
T1  - The Allele 2 of the VNTR Polymorphism in the Gene That Encodes a Natural Inhibitor of IL-1β, IL-1RA Is Favorably Associated With Chronic Otitis Media
VL  - 11
IS  - 2
SP  - 118
EP  - 123
DO  - 10.21053/ceo.2017.01060
ER  - 

@article{
author = "Živković, Maja and Kolić, Ivana and Ješić, Snežana and Jotić, Ana and Stanković, Aleksandra",
year = "2018",
abstract = "Objectives. Chronic otitis media (COM) is followed by irreversible tissue damage and destruction of the middle ear structures, with the possibility of complications under the maintenance of inflammation. Inflammatory mediators such as cytokines play a crucial role in the initial stage of inflammation. The aim of this study was to evaluate the association of the polymorphisms in two innate immunity/inflammation cascade genes from interleukin-1 (IL-1) gene cluster with COM with regard to cholesteatoma. Methods. In the cross-sectional case-control study, DNA samples were collected from 189 patients with COM and 119 controls from a population of Serbia. The +3953 C/T (rs1143634), TaqI polymorphism in interleukin-1 beta (IL-1Β) gene and 86 bp variable number tandem repeat (VNTR, rs2234663) polymorphism in the IL-1 receptor antagonist (IL-1RA) gene were analyzed by polymerase chain reaction. Results. The IL-1Β TaqI polymorphism was not significantly different in patients compared with the control group. The significant difference between patients and controls was observed for both, genotype and allele frequencies of IL-1RA VNTR polymorphism (chi-square P<0.01). We found that carriers of IL-1RA allele 2 (odds ratio, 0.47; 95% confidence interval, 0.29 to 0.76; P=0.004) have a favorable association with COM, using multivariate logistic analysis that included both polymorphisms, age and sex. The IL-1RA allele frequency distribution was significantly different with regard to cholesteatoma. Conclusion. The carriers of allele 2 of VNTR IL-1RA polymorphism had a decreased odds ratio for COM, which is in agreement with findings in other inflammatory disease and its previous association with higher IL-1RA levels. Possible down-regulation of IL-1 mediated proinflammatory signaling pathways via IL-1RA in COM as well as results of our study should be further investigated and replicated.",
journal = "Clinical and Experimental Otorhinolaryngology",
title = "The Allele 2 of the VNTR Polymorphism in the Gene That Encodes a Natural Inhibitor of IL-1β, IL-1RA Is Favorably Associated With Chronic Otitis Media",
volume = "11",
number = "2",
pages = "118-123",
doi = "10.21053/ceo.2017.01060"
}

Živković, M., Kolić, I., Ješić, S., Jotić, A.,& Stanković, A.. (2018). The Allele 2 of the VNTR Polymorphism in the Gene That Encodes a Natural Inhibitor of IL-1β, IL-1RA Is Favorably Associated With Chronic Otitis Media. in Clinical and Experimental Otorhinolaryngology, 11(2), 118-123.
https://doi.org/10.21053/ceo.2017.01060

Živković M, Kolić I, Ješić S, Jotić A, Stanković A. The Allele 2 of the VNTR Polymorphism in the Gene That Encodes a Natural Inhibitor of IL-1β, IL-1RA Is Favorably Associated With Chronic Otitis Media. in Clinical and Experimental Otorhinolaryngology. 2018;11(2):118-123.
doi:10.21053/ceo.2017.01060 .

Živković, Maja, Kolić, Ivana, Ješić, Snežana, Jotić, Ana, Stanković, Aleksandra, "The Allele 2 of the VNTR Polymorphism in the Gene That Encodes a Natural Inhibitor of IL-1β, IL-1RA Is Favorably Associated With Chronic Otitis Media" in Clinical and Experimental Otorhinolaryngology, 11, no. 2 (2018):118-123,
https://doi.org/10.21053/ceo.2017.01060 . .

TY  - CONF
AU  - Životić, Ivan
AU  - Jovanović, Ivan
AU  - Đurić, Tamara
AU  - Stanković, Aleksandra
AU  - Dekleva, Milica
AU  - Marković Nikolić, Nevena
AU  - Alavantić, Dragan
AU  - Živković, Maja
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/12816
AB  - Introduction: Recently, rs2275888 eQTL in PTPLAD2 gene has been associated with expression of several loci, during inflammatory stimulation in monocytes. Myocardial infarction (MI) triggers an intense inflammatory response that is essential for cardiac repair. We aimed to perform data scouting in appropriate rs2275888 genotype model to identify differentially expressed genes (DEGs), their biological meaning, and key miRs potentially associated with rs2275888 eQTL in peripheral blood mononuclear leucocytes (PBML) of MI patients 6 months after first MI. Methods: Transcriptome data was obtained from PBMLs of 21 patients, who suffered ischemic MI, by employing Illumina iScan microarray technology. Genotyping for rs2275888 was conducted with real-time PCR, using TaqMan® assay. Preprocessing and identification of DEGs was done using limma package of R/Bioconductor software. The online tool DAVID v6.8 was employed for functional enrichment analysis. Most important miRs were selected using NetworkAnalyst web tool, based on the degree centrality value. Results: Transcriptome analysis in recessive model TT+TC (n=19) vs. CC (n=2) identified 68 DEGs. Top significant biological processes involving DEGs cover vascular physiology, cell growth and signaling. Pathway analysis associated DEGs with adherens junction, Rap1 and Ras signaling. Network analysis identified hsa-miR335-5p, -26b-5p, -93-5p, -16-5p, -124-3p, -20b-5p, -17-5p and -218-5p as miRs with top centrality degree in our DEGs list. Conclusion: Seven of eight detected miRs have already been described in MI pathology or suggested as potential biomarkers for MI. Our result suggest the importance of integration of eQTLs, biological processes and pathway analysis coupled with miR activity for further research in MI pathology.
PB  - Belgrade : University of Belgrade, Faculty of Biology
C3  - CoMBoS1 - 1st Congress of Molecular Biologists of Serbia with international participation : Book of abstracts
T1  - Microarray transcriptome profiling in myocardial infarction regarding PTPLAD2 rs2275888 eQTL: a data scouting approach
SP  - 176
EP  - 176
UR  - https://hdl.handle.net/21.15107/rcub_vinar_12816
ER  - 

@conference{
author = "Životić, Ivan and Jovanović, Ivan and Đurić, Tamara and Stanković, Aleksandra and Dekleva, Milica and Marković Nikolić, Nevena and Alavantić, Dragan and Živković, Maja",
year = "2017",
abstract = "Introduction: Recently, rs2275888 eQTL in PTPLAD2 gene has been associated with expression of several loci, during inflammatory stimulation in monocytes. Myocardial infarction (MI) triggers an intense inflammatory response that is essential for cardiac repair. We aimed to perform data scouting in appropriate rs2275888 genotype model to identify differentially expressed genes (DEGs), their biological meaning, and key miRs potentially associated with rs2275888 eQTL in peripheral blood mononuclear leucocytes (PBML) of MI patients 6 months after first MI. Methods: Transcriptome data was obtained from PBMLs of 21 patients, who suffered ischemic MI, by employing Illumina iScan microarray technology. Genotyping for rs2275888 was conducted with real-time PCR, using TaqMan® assay. Preprocessing and identification of DEGs was done using limma package of R/Bioconductor software. The online tool DAVID v6.8 was employed for functional enrichment analysis. Most important miRs were selected using NetworkAnalyst web tool, based on the degree centrality value. Results: Transcriptome analysis in recessive model TT+TC (n=19) vs. CC (n=2) identified 68 DEGs. Top significant biological processes involving DEGs cover vascular physiology, cell growth and signaling. Pathway analysis associated DEGs with adherens junction, Rap1 and Ras signaling. Network analysis identified hsa-miR335-5p, -26b-5p, -93-5p, -16-5p, -124-3p, -20b-5p, -17-5p and -218-5p as miRs with top centrality degree in our DEGs list. Conclusion: Seven of eight detected miRs have already been described in MI pathology or suggested as potential biomarkers for MI. Our result suggest the importance of integration of eQTLs, biological processes and pathway analysis coupled with miR activity for further research in MI pathology.",
publisher = "Belgrade : University of Belgrade, Faculty of Biology",
journal = "CoMBoS1 - 1st Congress of Molecular Biologists of Serbia with international participation : Book of abstracts",
title = "Microarray transcriptome profiling in myocardial infarction regarding PTPLAD2 rs2275888 eQTL: a data scouting approach",
pages = "176-176",
url = "https://hdl.handle.net/21.15107/rcub_vinar_12816"
}

Životić, I., Jovanović, I., Đurić, T., Stanković, A., Dekleva, M., Marković Nikolić, N., Alavantić, D.,& Živković, M.. (2017). Microarray transcriptome profiling in myocardial infarction regarding PTPLAD2 rs2275888 eQTL: a data scouting approach. in CoMBoS1 - 1st Congress of Molecular Biologists of Serbia with international participation : Book of abstracts
Belgrade : University of Belgrade, Faculty of Biology., 176-176.
https://hdl.handle.net/21.15107/rcub_vinar_12816

Životić I, Jovanović I, Đurić T, Stanković A, Dekleva M, Marković Nikolić N, Alavantić D, Živković M. Microarray transcriptome profiling in myocardial infarction regarding PTPLAD2 rs2275888 eQTL: a data scouting approach. in CoMBoS1 - 1st Congress of Molecular Biologists of Serbia with international participation : Book of abstracts. 2017;:176-176.
https://hdl.handle.net/21.15107/rcub_vinar_12816 .

Životić, Ivan, Jovanović, Ivan, Đurić, Tamara, Stanković, Aleksandra, Dekleva, Milica, Marković Nikolić, Nevena, Alavantić, Dragan, Živković, Maja, "Microarray transcriptome profiling in myocardial infarction regarding PTPLAD2 rs2275888 eQTL: a data scouting approach" in CoMBoS1 - 1st Congress of Molecular Biologists of Serbia with international participation : Book of abstracts (2017):176-176,
https://hdl.handle.net/21.15107/rcub_vinar_12816 .

TY  - JOUR
AU  - Bundalo, Maja M.
AU  - Romić, Snježana Đ.
AU  - Tepavčević, Snežana
AU  - Stojiljković, Mojca D.
AU  - Stanković, Aleksandra
AU  - Živković, Maja
AU  - Korićanac, Goran
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1726
AB  - Increased intake of fructose in humans and laboratory animals is demonstrated to be a risk factor for development of metabolic disorders (insulin resistance, metabolic syndrome, type 2 diabetes) and cardiovascular diseases. On the other hand, estradiol is emphasized as a cardioprotective agent. The main goal of this review is to summarize recent findings on damaging cardiac effects of fructose-rich diet in females, mostly experimental animals, and to evaluate protective capacity of estradiol. Published results of our and other research groups indicate mostly detrimental effects of fructose-rich diet on cardiac insulin signaling molecules, glucose and fatty acid metabolism, nitric oxide production and ion transport, as well as renin-angiotensin system and inflammation. Some of these processes are involved in cardiac insulin signal transmission, others are regulated by insulin or have an influence on insulin action. Administration of estradiol to ovariectomized female rats, exposed to increased intake of fructose, was mostly beneficial to the heart, but sometimes it was ineffective or even detrimental, depending on the particular processes. We believe that these data, carefully translated to human population, could be useful for clinicians dealing with postmenopausal women susceptible to metabolic diseases and hormone replacement therapy.
T2  - European Journal of Pharmacology
T1  - Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe?
VL  - 811
SP  - 141
EP  - 147
DO  - 10.1016/j.ejphar.2017.06.003
ER  - 

@article{
author = "Bundalo, Maja M. and Romić, Snježana Đ. and Tepavčević, Snežana and Stojiljković, Mojca D. and Stanković, Aleksandra and Živković, Maja and Korićanac, Goran",
year = "2017",
abstract = "Increased intake of fructose in humans and laboratory animals is demonstrated to be a risk factor for development of metabolic disorders (insulin resistance, metabolic syndrome, type 2 diabetes) and cardiovascular diseases. On the other hand, estradiol is emphasized as a cardioprotective agent. The main goal of this review is to summarize recent findings on damaging cardiac effects of fructose-rich diet in females, mostly experimental animals, and to evaluate protective capacity of estradiol. Published results of our and other research groups indicate mostly detrimental effects of fructose-rich diet on cardiac insulin signaling molecules, glucose and fatty acid metabolism, nitric oxide production and ion transport, as well as renin-angiotensin system and inflammation. Some of these processes are involved in cardiac insulin signal transmission, others are regulated by insulin or have an influence on insulin action. Administration of estradiol to ovariectomized female rats, exposed to increased intake of fructose, was mostly beneficial to the heart, but sometimes it was ineffective or even detrimental, depending on the particular processes. We believe that these data, carefully translated to human population, could be useful for clinicians dealing with postmenopausal women susceptible to metabolic diseases and hormone replacement therapy.",
journal = "European Journal of Pharmacology",
title = "Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe?",
volume = "811",
pages = "141-147",
doi = "10.1016/j.ejphar.2017.06.003"
}

Bundalo, M. M., Romić, S. Đ., Tepavčević, S., Stojiljković, M. D., Stanković, A., Živković, M.,& Korićanac, G.. (2017). Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe?. in European Journal of Pharmacology, 811, 141-147.
https://doi.org/10.1016/j.ejphar.2017.06.003

Bundalo MM, Romić SĐ, Tepavčević S, Stojiljković MD, Stanković A, Živković M, Korićanac G. Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe?. in European Journal of Pharmacology. 2017;811:141-147.
doi:10.1016/j.ejphar.2017.06.003 .

Bundalo, Maja M., Romić, Snježana Đ., Tepavčević, Snežana, Stojiljković, Mojca D., Stanković, Aleksandra, Živković, Maja, Korićanac, Goran, "Fructose-rich diet and insulin action in female rat heart: Estradiol friend or foe?" in European Journal of Pharmacology, 811 (2017):141-147,
https://doi.org/10.1016/j.ejphar.2017.06.003 . .

TY  - JOUR
AU  - Bundalo, Maja M.
AU  - Đorđević, Ana D.
AU  - Bursać, Biljana
AU  - Živković, Maja
AU  - Korićanac, Goran
AU  - Stanković, Aleksandra
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1839
AB  - The adipose tissue renin-angiotensin system (RAS) is proposed to be a pathophysiological link between adipose tissue dysregulation and metabolic disorders induced by a fructose-rich diet (FRD). RAS can act intracellularly. We hypothesized that adipocyte nuclear membranes possess angiotensin receptor types 1 and 2 (AT1R and AT2R), which couple to nuclear signaling pathways and regulate oxidative gene expression under FRD conditions. We analyzed the effect of consumption of 10% fructose solution for 9 weeks on biochemical parameters, adipocyte morphology, and expression of AT1R, AT2R, AT1R-associated protein (ATRAP), NADPH oxidase 4 (NOX4), matrix metalloproteinase-9 (MMP-9), and manganese superoxide dismutase (MnSOD) in adipose tissue of Wistar rats. We detected AT1R and AT2R in the nuclear fraction. FRD reduced the level of angiotensin receptors in the nucleus, while increased AT1R and decreased AT2R levels were observed in the plasma membrane. FRD increased the ATRAP mRNA level and decreased MnSOD mRNA and protein levels. No significant differences were observed for MMP-9 and NOX4 mRNA levels. These findings coincided with hyperleptinemia, elevated blood pressure and triglycerides, and unchanged visceral adipose tissue mass and morphology in FRD rats. Besides providing evidence for nuclear localization of angiotensin receptors in visceral adipose tissue, this study demonstrates the different effects of FRD on AT1R expression in different cellular compartments. Elevated blood pressure and decreased antioxidant capacity in visceral fat of fructose-fed rats were accompanied by an increased AT1R level in the plasma membrane, while upregulation of ATRAP and a decrease of nuclear membrane AT1R suggest an increased capacity for attenuation of excessive AT1R signaling and visceral adiposity.
T2  - Applied Physiology Nutrition and Metabolism
T1  - Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue
VL  - 42
IS  - 12
SP  - 1254
EP  - 1263
DO  - 10.1139/apnm-2016-0725
ER  - 

@article{
author = "Bundalo, Maja M. and Đorđević, Ana D. and Bursać, Biljana and Živković, Maja and Korićanac, Goran and Stanković, Aleksandra",
year = "2017",
abstract = "The adipose tissue renin-angiotensin system (RAS) is proposed to be a pathophysiological link between adipose tissue dysregulation and metabolic disorders induced by a fructose-rich diet (FRD). RAS can act intracellularly. We hypothesized that adipocyte nuclear membranes possess angiotensin receptor types 1 and 2 (AT1R and AT2R), which couple to nuclear signaling pathways and regulate oxidative gene expression under FRD conditions. We analyzed the effect of consumption of 10% fructose solution for 9 weeks on biochemical parameters, adipocyte morphology, and expression of AT1R, AT2R, AT1R-associated protein (ATRAP), NADPH oxidase 4 (NOX4), matrix metalloproteinase-9 (MMP-9), and manganese superoxide dismutase (MnSOD) in adipose tissue of Wistar rats. We detected AT1R and AT2R in the nuclear fraction. FRD reduced the level of angiotensin receptors in the nucleus, while increased AT1R and decreased AT2R levels were observed in the plasma membrane. FRD increased the ATRAP mRNA level and decreased MnSOD mRNA and protein levels. No significant differences were observed for MMP-9 and NOX4 mRNA levels. These findings coincided with hyperleptinemia, elevated blood pressure and triglycerides, and unchanged visceral adipose tissue mass and morphology in FRD rats. Besides providing evidence for nuclear localization of angiotensin receptors in visceral adipose tissue, this study demonstrates the different effects of FRD on AT1R expression in different cellular compartments. Elevated blood pressure and decreased antioxidant capacity in visceral fat of fructose-fed rats were accompanied by an increased AT1R level in the plasma membrane, while upregulation of ATRAP and a decrease of nuclear membrane AT1R suggest an increased capacity for attenuation of excessive AT1R signaling and visceral adiposity.",
journal = "Applied Physiology Nutrition and Metabolism",
title = "Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue",
volume = "42",
number = "12",
pages = "1254-1263",
doi = "10.1139/apnm-2016-0725"
}

Bundalo, M. M., Đorđević, A. D., Bursać, B., Živković, M., Korićanac, G.,& Stanković, A.. (2017). Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue. in Applied Physiology Nutrition and Metabolism, 42(12), 1254-1263.
https://doi.org/10.1139/apnm-2016-0725

Bundalo MM, Đorđević AD, Bursać B, Živković M, Korićanac G, Stanković A. Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue. in Applied Physiology Nutrition and Metabolism. 2017;42(12):1254-1263.
doi:10.1139/apnm-2016-0725 .

Bundalo, Maja M., Đorđević, Ana D., Bursać, Biljana, Živković, Maja, Korićanac, Goran, Stanković, Aleksandra, "Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue" in Applied Physiology Nutrition and Metabolism, 42, no. 12 (2017):1254-1263,
https://doi.org/10.1139/apnm-2016-0725 . .

TY  - JOUR
AU  - Cvetković, Mirjana
AU  - Živković, Maja
AU  - Bundalo, Maja M.
AU  - Gojković, Ivana
AU  - Spasojević-Dimitrijeva, Brankica
AU  - Stanković, Aleksandra
AU  - Kostić, Mirjana M.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1918
AB  - Background: The interindividual variability of cyclosporin A (CsA) pharmacokinetics might be explained by heterogeneity in the cytochrome P450 3A (CYP3A) subfamily. Altered CYP3A enzyme activity was associated with variant allele of P450 oxidoreductase gene (POR*28). The aim of this study was to assess the impact of age, CYP3A5*3, CYP3A4*22, and POR*28 alleles on CsA pharmacokinetics in pediatric renal transplant recipients. Methods: Renal transplant patients receiving CsA (n = 47) were genotyped for CYP3A5*3, CYP3A4*22, and POR*28. Results: CYP3A5 nonexpressers had higher overall dose-adjusted predose concentration (C0/dose; ng/mL per mg/kg) compared with expressers (31.48 +/- 12.75 versus 22.44 +/- 7.12, P = 0.01). CY-P3A5 nonexpressers carrying POR*28 allele had a lower overall dose-adjusted concentration (C2/dose) than those with POR*1/*1 genotype (165.54 +/- 70.40 versus 210.55 +/- 79.98, P = 0.02), with age as covariate. Children aged 6 years and younger had a lower overall C0/dose (18.82 +/- 4.72 versus 34.19 +/- 11.89, P = 0.001) and C2/dose (106.75 +/- 26.99 versus 209.20 +/- 71.57, P LT 0.001) compared with older children. Carriers of CYP3A5*3 allele aged LT = 6 years required higher dose of CsA and achieved lower C0/dose and C2/dose, at most time points, than older carriers of this allele. Carriers of POR*28 allele aged # 6 years required higher doses of CsA, whereas they achieved lower C0/dose and C2/dose, at most time points, in comparison to older carriers of this allele. The significant effect of age (P LT 0.002) and CYP3A5 variation (P, 0.02) was shown for overall C0/dose, whereas age (P LT 0.00001) and POR variation (P = 0.05) showed significant effect on C2/dose. Regression summary for overall C2/dose in patients aged 6 years younger showed a significant effect of both CYP3A5 and POR variations (P LT 0.016). Conclusions: Younger age, POR*28 allele, and CYP3A5*3 allele were associated with higher CsA dosing requirements and lower concentration/dose ratio. Pretransplant screening of relevant polymorphisms in accordance with age should be considered to adjust therapy.
T2  - Therapeutic Drug Monitoring
T1  - Effect of Age and Allele Variants of CYP3A5, CYP3A4, and POR Genes on the Pharmacokinetics of Cyclosporin A in Pediatric Renal Transplant Recipients From Serbia
VL  - 39
IS  - 6
SP  - 589
EP  - 595
DO  - 10.1097/FTD.0000000000000442
ER  - 

@article{
author = "Cvetković, Mirjana and Živković, Maja and Bundalo, Maja M. and Gojković, Ivana and Spasojević-Dimitrijeva, Brankica and Stanković, Aleksandra and Kostić, Mirjana M.",
year = "2017",
abstract = "Background: The interindividual variability of cyclosporin A (CsA) pharmacokinetics might be explained by heterogeneity in the cytochrome P450 3A (CYP3A) subfamily. Altered CYP3A enzyme activity was associated with variant allele of P450 oxidoreductase gene (POR*28). The aim of this study was to assess the impact of age, CYP3A5*3, CYP3A4*22, and POR*28 alleles on CsA pharmacokinetics in pediatric renal transplant recipients. Methods: Renal transplant patients receiving CsA (n = 47) were genotyped for CYP3A5*3, CYP3A4*22, and POR*28. Results: CYP3A5 nonexpressers had higher overall dose-adjusted predose concentration (C0/dose; ng/mL per mg/kg) compared with expressers (31.48 +/- 12.75 versus 22.44 +/- 7.12, P = 0.01). CY-P3A5 nonexpressers carrying POR*28 allele had a lower overall dose-adjusted concentration (C2/dose) than those with POR*1/*1 genotype (165.54 +/- 70.40 versus 210.55 +/- 79.98, P = 0.02), with age as covariate. Children aged 6 years and younger had a lower overall C0/dose (18.82 +/- 4.72 versus 34.19 +/- 11.89, P = 0.001) and C2/dose (106.75 +/- 26.99 versus 209.20 +/- 71.57, P LT 0.001) compared with older children. Carriers of CYP3A5*3 allele aged LT = 6 years required higher dose of CsA and achieved lower C0/dose and C2/dose, at most time points, than older carriers of this allele. Carriers of POR*28 allele aged # 6 years required higher doses of CsA, whereas they achieved lower C0/dose and C2/dose, at most time points, in comparison to older carriers of this allele. The significant effect of age (P LT 0.002) and CYP3A5 variation (P, 0.02) was shown for overall C0/dose, whereas age (P LT 0.00001) and POR variation (P = 0.05) showed significant effect on C2/dose. Regression summary for overall C2/dose in patients aged 6 years younger showed a significant effect of both CYP3A5 and POR variations (P LT 0.016). Conclusions: Younger age, POR*28 allele, and CYP3A5*3 allele were associated with higher CsA dosing requirements and lower concentration/dose ratio. Pretransplant screening of relevant polymorphisms in accordance with age should be considered to adjust therapy.",
journal = "Therapeutic Drug Monitoring",
title = "Effect of Age and Allele Variants of CYP3A5, CYP3A4, and POR Genes on the Pharmacokinetics of Cyclosporin A in Pediatric Renal Transplant Recipients From Serbia",
volume = "39",
number = "6",
pages = "589-595",
doi = "10.1097/FTD.0000000000000442"
}

Cvetković, M., Živković, M., Bundalo, M. M., Gojković, I., Spasojević-Dimitrijeva, B., Stanković, A.,& Kostić, M. M.. (2017). Effect of Age and Allele Variants of CYP3A5, CYP3A4, and POR Genes on the Pharmacokinetics of Cyclosporin A in Pediatric Renal Transplant Recipients From Serbia. in Therapeutic Drug Monitoring, 39(6), 589-595.
https://doi.org/10.1097/FTD.0000000000000442

Cvetković M, Živković M, Bundalo MM, Gojković I, Spasojević-Dimitrijeva B, Stanković A, Kostić MM. Effect of Age and Allele Variants of CYP3A5, CYP3A4, and POR Genes on the Pharmacokinetics of Cyclosporin A in Pediatric Renal Transplant Recipients From Serbia. in Therapeutic Drug Monitoring. 2017;39(6):589-595.
doi:10.1097/FTD.0000000000000442 .

Cvetković, Mirjana, Živković, Maja, Bundalo, Maja M., Gojković, Ivana, Spasojević-Dimitrijeva, Brankica, Stanković, Aleksandra, Kostić, Mirjana M., "Effect of Age and Allele Variants of CYP3A5, CYP3A4, and POR Genes on the Pharmacokinetics of Cyclosporin A in Pediatric Renal Transplant Recipients From Serbia" in Therapeutic Drug Monitoring, 39, no. 6 (2017):589-595,
https://doi.org/10.1097/FTD.0000000000000442 . .

TY  - JOUR
AU  - Živković, Maja
AU  - Kolaković, Ana
AU  - Stojković, Ljiljana S.
AU  - Dinčić, Evica
AU  - Kostic, Smiljana
AU  - Alavantić, Dragan
AU  - Stanković, Aleksandra
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1016
AB  - The components of renin-angiotensin system, such as angiotensin-converting enzyme (ACE), angiotensin II and angiotensin II receptor type 1 and 2 (AT1R and AT2R), are expressed in the central nervous system and leukocytes and proposed to be involved in the inflammation and pathogenesis of multiple sclerosis (MS). ACE I/D, AT1R 1166A/C and AT2R-1332A/G are functional polymorphisms associated with phenotypes of diverse chronic inflammatory diseases. The aim of this study was to investigate the association between ACE I/D, AT1R 1166A/C and AT2R-1332A/G gene polymorphisms and MS in Serbian population. A total of 470 MS patients and 478 controls participated in the study. Allele-specific polymerase chain reaction (PCR) was performed for genotyping of the ACE polymorphism. The AT1R and AT2R genotyping was done by duplex PCR and restriction fragment length polymorphism analysis. Both ACE homozygotes, II and DD, were significantly overrepresented in MS patients, compared to controls (chi(2) test p = 0.03). Neither genotype nor allele frequencies of AT1R 1166A/C polymorphism were significantly different between patients and controls. Significant overrepresentation of AT2R-1332 AA genotype in female patients, compared to female controls, was detected (OR = 1.67, 95%CI = 1.13-2.49, chi(2) test p = 0.01), suggesting that this genotype could be a gender-specific genetic risk factor for MS. (C) 2016 Elsevier B.V. All rights reserved.
T2  - Journal of the Neurological Sciences
T1  - Renin-angiotensin system gene polymorphisms as risk factors for multiple sclerosis
VL  - 363
SP  - 29
EP  - 32
DO  - 10.1016/j.jns.2016.02.026
ER  - 

@article{
author = "Živković, Maja and Kolaković, Ana and Stojković, Ljiljana S. and Dinčić, Evica and Kostic, Smiljana and Alavantić, Dragan and Stanković, Aleksandra",
year = "2016",
abstract = "The components of renin-angiotensin system, such as angiotensin-converting enzyme (ACE), angiotensin II and angiotensin II receptor type 1 and 2 (AT1R and AT2R), are expressed in the central nervous system and leukocytes and proposed to be involved in the inflammation and pathogenesis of multiple sclerosis (MS). ACE I/D, AT1R 1166A/C and AT2R-1332A/G are functional polymorphisms associated with phenotypes of diverse chronic inflammatory diseases. The aim of this study was to investigate the association between ACE I/D, AT1R 1166A/C and AT2R-1332A/G gene polymorphisms and MS in Serbian population. A total of 470 MS patients and 478 controls participated in the study. Allele-specific polymerase chain reaction (PCR) was performed for genotyping of the ACE polymorphism. The AT1R and AT2R genotyping was done by duplex PCR and restriction fragment length polymorphism analysis. Both ACE homozygotes, II and DD, were significantly overrepresented in MS patients, compared to controls (chi(2) test p = 0.03). Neither genotype nor allele frequencies of AT1R 1166A/C polymorphism were significantly different between patients and controls. Significant overrepresentation of AT2R-1332 AA genotype in female patients, compared to female controls, was detected (OR = 1.67, 95%CI = 1.13-2.49, chi(2) test p = 0.01), suggesting that this genotype could be a gender-specific genetic risk factor for MS. (C) 2016 Elsevier B.V. All rights reserved.",
journal = "Journal of the Neurological Sciences",
title = "Renin-angiotensin system gene polymorphisms as risk factors for multiple sclerosis",
volume = "363",
pages = "29-32",
doi = "10.1016/j.jns.2016.02.026"
}

Živković, M., Kolaković, A., Stojković, L. S., Dinčić, E., Kostic, S., Alavantić, D.,& Stanković, A.. (2016). Renin-angiotensin system gene polymorphisms as risk factors for multiple sclerosis. in Journal of the Neurological Sciences, 363, 29-32.
https://doi.org/10.1016/j.jns.2016.02.026

Živković M, Kolaković A, Stojković LS, Dinčić E, Kostic S, Alavantić D, Stanković A. Renin-angiotensin system gene polymorphisms as risk factors for multiple sclerosis. in Journal of the Neurological Sciences. 2016;363:29-32.
doi:10.1016/j.jns.2016.02.026 .

Živković, Maja, Kolaković, Ana, Stojković, Ljiljana S., Dinčić, Evica, Kostic, Smiljana, Alavantić, Dragan, Stanković, Aleksandra, "Renin-angiotensin system gene polymorphisms as risk factors for multiple sclerosis" in Journal of the Neurological Sciences, 363 (2016):29-32,
https://doi.org/10.1016/j.jns.2016.02.026 . .

TY  - JOUR
AU  - Petrović, Nina
AU  - Kolaković, Ana
AU  - Stanković, Aleksandra
AU  - Lukić, Silvana
AU  - Sami, Ahmad
AU  - Živković, Maja
AU  - Mandušić, Vesna
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1023
AB  - BACKGROUND: Breast carcinoma is heterogeneous disease. Understanding the process of invasion and metastasis and the selection of the therapy for patients with breast carcinomas still remains difficult. MicroRNAs are powerful gene expression regulators. Because of inconsistent findings, we have analyzed potential difference in miR-155 levels in three breast cancer groups. OBJECTIVES: Our goals were to examine miR-155 expression levels in normal tissue, non-invasive and invasive breast carcinomas, and their association with standard clinical and pathological parameters and oncomiR-21, and to investigate the ability of miR-155 to separate invasive breast carcinomas with non-invasive component from pure invasive. METHODS: In the group of 40 breast tissue samples, relative expression levels of miR-155 were examined with stem-loop quantitative real-time PCR using TaqMan technology. RESULTS: The significant difference among four examined groups of the breast tissue was detected (p = 0.001). In the group of pure invasive tumors, patients with positive nodal status had significantly higher miR-155 levels (p = 0.046). CONCLUSION: Our results suggest that miR-155 might be involved in breast cancer pathogenesis and in tumor spreading to the lymph nodes, and that it might be used as biomarker for additional stratification of patients with invasive breast carcinomas with non-invasive component.
T2  - Cancer Biomarkers
T1  - miR-155 expression level changes might be associated with initial phases of breast cancer pathogenesis and lymph-node metastasis
VL  - 16
IS  - 3
SP  - 385
EP  - 394
DO  - 10.3233/CBM-160577
ER  - 

@article{
author = "Petrović, Nina and Kolaković, Ana and Stanković, Aleksandra and Lukić, Silvana and Sami, Ahmad and Živković, Maja and Mandušić, Vesna",
year = "2016",
abstract = "BACKGROUND: Breast carcinoma is heterogeneous disease. Understanding the process of invasion and metastasis and the selection of the therapy for patients with breast carcinomas still remains difficult. MicroRNAs are powerful gene expression regulators. Because of inconsistent findings, we have analyzed potential difference in miR-155 levels in three breast cancer groups. OBJECTIVES: Our goals were to examine miR-155 expression levels in normal tissue, non-invasive and invasive breast carcinomas, and their association with standard clinical and pathological parameters and oncomiR-21, and to investigate the ability of miR-155 to separate invasive breast carcinomas with non-invasive component from pure invasive. METHODS: In the group of 40 breast tissue samples, relative expression levels of miR-155 were examined with stem-loop quantitative real-time PCR using TaqMan technology. RESULTS: The significant difference among four examined groups of the breast tissue was detected (p = 0.001). In the group of pure invasive tumors, patients with positive nodal status had significantly higher miR-155 levels (p = 0.046). CONCLUSION: Our results suggest that miR-155 might be involved in breast cancer pathogenesis and in tumor spreading to the lymph nodes, and that it might be used as biomarker for additional stratification of patients with invasive breast carcinomas with non-invasive component.",
journal = "Cancer Biomarkers",
title = "miR-155 expression level changes might be associated with initial phases of breast cancer pathogenesis and lymph-node metastasis",
volume = "16",
number = "3",
pages = "385-394",
doi = "10.3233/CBM-160577"
}

Petrović, N., Kolaković, A., Stanković, A., Lukić, S., Sami, A., Živković, M.,& Mandušić, V.. (2016). miR-155 expression level changes might be associated with initial phases of breast cancer pathogenesis and lymph-node metastasis. in Cancer Biomarkers, 16(3), 385-394.
https://doi.org/10.3233/CBM-160577

Petrović N, Kolaković A, Stanković A, Lukić S, Sami A, Živković M, Mandušić V. miR-155 expression level changes might be associated with initial phases of breast cancer pathogenesis and lymph-node metastasis. in Cancer Biomarkers. 2016;16(3):385-394.
doi:10.3233/CBM-160577 .

Petrović, Nina, Kolaković, Ana, Stanković, Aleksandra, Lukić, Silvana, Sami, Ahmad, Živković, Maja, Mandušić, Vesna, "miR-155 expression level changes might be associated with initial phases of breast cancer pathogenesis and lymph-node metastasis" in Cancer Biomarkers, 16, no. 3 (2016):385-394,
https://doi.org/10.3233/CBM-160577 . .

TY  - JOUR
AU  - Stanković, Aleksandra
AU  - Kolaković, Ana
AU  - Živković, Maja
AU  - Đurić, Tamara
AU  - Bundalo, Maja M.
AU  - Končar, Igor
AU  - Davidović, Lazar
AU  - Alavantić, Dragan
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1045
AB  - Background and Aims: The principal biologic effects of the renin-angiotensin system are mediated by activation of the AT1R receptor. The microRNA miR-155 regulates AT1R expression, with both its, and AT1Rs activity, linked to atherosclerosis. Target sites for miR-155 lie within the 3 UTR of the human AT1R gene, and include the AT1R A1166C polymorphism. Thus far, only levels of circulating miR-155 have been investigated with respect to A1166C genotypes. We hypothesized that the A1166C polymorphism could correlate with different, ultra-sonographically defined plaque phenotypes, as well as with an altered expression of AT1R mRNA and protein in human carotid plaques (CP), and altered expression of miR-155 in patients with advanced atherosclerosis. Methods: Our study cohort comprised 411 patients with advanced carotid atherosclerosis (298 hyperechoic; 113 hypoechoic plaques). PCR analyses identified A1166C genotypes; quantitative real-time PCR determined AT1R and miR-155 expression levels, with AT1R protein expression evaluated by western blot. Results: Genotypes containing the C allele bore a significant association with the hypoechoic plaque phenotype (adjusted OR 1.87, 95% CI 1.16-3.00, p = 0.01). The expression of AT1R mRNA and miR-155 were significantly up-regulated in the CPs of CC genotype carriers compared to the AA/AC genotypes (p = 0.032, p = 0.015, respectively). AT1R protein expression was also significantly higher for CC genotypes (p LT 0.01). Conclusion: Our results indicate that the AT1R A1166C polymorphism impacts an ultrasonographicallydefined human plaque phenotype, with intra-plaque AT1R and miR-155 expression altered in advanced carotid atherosclerosis. Validation and replication of these data should contribute to an improved personalized therapy with which to prevent carotid atherosclerosis. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
PB  - Elsevier
T2  - Atherosclerosis
T1  - Angiotensin receptor type 1 polymorphism A1166C is associated with altered AT1R and miR-155 expression in carotid plaque tissue and development of hypoechoic carotid plaques
VL  - 248
SP  - 132
EP  - 139
DO  - 10.1016/j.atherosclerosis.2016.02.032
ER  - 

@article{
author = "Stanković, Aleksandra and Kolaković, Ana and Živković, Maja and Đurić, Tamara and Bundalo, Maja M. and Končar, Igor and Davidović, Lazar and Alavantić, Dragan",
year = "2016",
abstract = "Background and Aims: The principal biologic effects of the renin-angiotensin system are mediated by activation of the AT1R receptor. The microRNA miR-155 regulates AT1R expression, with both its, and AT1Rs activity, linked to atherosclerosis. Target sites for miR-155 lie within the 3 UTR of the human AT1R gene, and include the AT1R A1166C polymorphism. Thus far, only levels of circulating miR-155 have been investigated with respect to A1166C genotypes. We hypothesized that the A1166C polymorphism could correlate with different, ultra-sonographically defined plaque phenotypes, as well as with an altered expression of AT1R mRNA and protein in human carotid plaques (CP), and altered expression of miR-155 in patients with advanced atherosclerosis. Methods: Our study cohort comprised 411 patients with advanced carotid atherosclerosis (298 hyperechoic; 113 hypoechoic plaques). PCR analyses identified A1166C genotypes; quantitative real-time PCR determined AT1R and miR-155 expression levels, with AT1R protein expression evaluated by western blot. Results: Genotypes containing the C allele bore a significant association with the hypoechoic plaque phenotype (adjusted OR 1.87, 95% CI 1.16-3.00, p = 0.01). The expression of AT1R mRNA and miR-155 were significantly up-regulated in the CPs of CC genotype carriers compared to the AA/AC genotypes (p = 0.032, p = 0.015, respectively). AT1R protein expression was also significantly higher for CC genotypes (p LT 0.01). Conclusion: Our results indicate that the AT1R A1166C polymorphism impacts an ultrasonographicallydefined human plaque phenotype, with intra-plaque AT1R and miR-155 expression altered in advanced carotid atherosclerosis. Validation and replication of these data should contribute to an improved personalized therapy with which to prevent carotid atherosclerosis. (C) 2016 Elsevier Ireland Ltd. All rights reserved.",
publisher = "Elsevier",
journal = "Atherosclerosis",
title = "Angiotensin receptor type 1 polymorphism A1166C is associated with altered AT1R and miR-155 expression in carotid plaque tissue and development of hypoechoic carotid plaques",
volume = "248",
pages = "132-139",
doi = "10.1016/j.atherosclerosis.2016.02.032"
}

Stanković, A., Kolaković, A., Živković, M., Đurić, T., Bundalo, M. M., Končar, I., Davidović, L.,& Alavantić, D.. (2016). Angiotensin receptor type 1 polymorphism A1166C is associated with altered AT1R and miR-155 expression in carotid plaque tissue and development of hypoechoic carotid plaques. in Atherosclerosis
Elsevier., 248, 132-139.
https://doi.org/10.1016/j.atherosclerosis.2016.02.032

Stanković A, Kolaković A, Živković M, Đurić T, Bundalo MM, Končar I, Davidović L, Alavantić D. Angiotensin receptor type 1 polymorphism A1166C is associated with altered AT1R and miR-155 expression in carotid plaque tissue and development of hypoechoic carotid plaques. in Atherosclerosis. 2016;248:132-139.
doi:10.1016/j.atherosclerosis.2016.02.032 .

Stanković, Aleksandra, Kolaković, Ana, Živković, Maja, Đurić, Tamara, Bundalo, Maja M., Končar, Igor, Davidović, Lazar, Alavantić, Dragan, "Angiotensin receptor type 1 polymorphism A1166C is associated with altered AT1R and miR-155 expression in carotid plaque tissue and development of hypoechoic carotid plaques" in Atherosclerosis, 248 (2016):132-139,
https://doi.org/10.1016/j.atherosclerosis.2016.02.032 . .

TY  - JOUR
AU  - Kolaković, Ana
AU  - Stanković, Aleksandra
AU  - Đurić, Tamara
AU  - Živković, Maja
AU  - Končar, Igor
AU  - Davidović, Lazar
AU  - Radak, Đorđe J.
AU  - Alavantić, Dragan
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1123
AB  - Background: The angiotensin II type 2 receptor (AT2R) - 1332 A/G polymorphism has been denoted as functional and associated with certain cardiovascular disease phenotypes. However, there are no studies considering the association of this gene polymorphism with carotid atherosclerosis (CA) and cerebrovascular events. Therefore, the aim of our study was to investigate a possible association of the AT2R - 1332 A/G polymorphism with the occurrence of carotid plaques (CPs) and history of cerebrovascular insult (CVI) in advanced CA. Methods: The study group included 381 controls and 509 patients with CA consecutively admitted for endarterectomy. Genotyping was determined by polymerase chain reaction-restriction fragment length polymorphism method. The association was analyzed separately for males and females because the AT2R gene is located on the X chromosome. Results: The AT2R - 1332 GG genotype was associated with the advanced CA in the female study group (recessive model of inheritance, AA+AG versus GG; adjusted odds ratio [OR] = 2.25; 95% confidence interval [CI] 1.17-4.33; P=.01). In the male subgroup of patients with CA, the significant overrepresentation of G/- hemizygote was detected in patients with CVI compared to male patients without this event (crude OR = 2.05, 95% CI 1.20-3.50, P=.008). Conclusions: This study suggests a gender-specific association between the AT2R -1332 A/G polymorphism and the occurrence of CP and the history of CVI in advanced CA, but further replication studies are needed. (C) 2016 National Stroke Association. Published by Elsevier Inc. All rights reserved.
T2  - Journal of Stroke and Cerebrovascular Diseases
T1  - Gender-Specific Association between Angiotensin II Type 2 Receptor-1332 A/G Gene Polymorphism and Advanced Carotid Atherosclerosis
VL  - 25
IS  - 7
SP  - 1622
EP  - 1630
DO  - 10.1016/j.jstrokecerebrovasdis.2016.03.011
ER  - 

@article{
author = "Kolaković, Ana and Stanković, Aleksandra and Đurić, Tamara and Živković, Maja and Končar, Igor and Davidović, Lazar and Radak, Đorđe J. and Alavantić, Dragan",
year = "2016",
abstract = "Background: The angiotensin II type 2 receptor (AT2R) - 1332 A/G polymorphism has been denoted as functional and associated with certain cardiovascular disease phenotypes. However, there are no studies considering the association of this gene polymorphism with carotid atherosclerosis (CA) and cerebrovascular events. Therefore, the aim of our study was to investigate a possible association of the AT2R - 1332 A/G polymorphism with the occurrence of carotid plaques (CPs) and history of cerebrovascular insult (CVI) in advanced CA. Methods: The study group included 381 controls and 509 patients with CA consecutively admitted for endarterectomy. Genotyping was determined by polymerase chain reaction-restriction fragment length polymorphism method. The association was analyzed separately for males and females because the AT2R gene is located on the X chromosome. Results: The AT2R - 1332 GG genotype was associated with the advanced CA in the female study group (recessive model of inheritance, AA+AG versus GG; adjusted odds ratio [OR] = 2.25; 95% confidence interval [CI] 1.17-4.33; P=.01). In the male subgroup of patients with CA, the significant overrepresentation of G/- hemizygote was detected in patients with CVI compared to male patients without this event (crude OR = 2.05, 95% CI 1.20-3.50, P=.008). Conclusions: This study suggests a gender-specific association between the AT2R -1332 A/G polymorphism and the occurrence of CP and the history of CVI in advanced CA, but further replication studies are needed. (C) 2016 National Stroke Association. Published by Elsevier Inc. All rights reserved.",
journal = "Journal of Stroke and Cerebrovascular Diseases",
title = "Gender-Specific Association between Angiotensin II Type 2 Receptor-1332 A/G Gene Polymorphism and Advanced Carotid Atherosclerosis",
volume = "25",
number = "7",
pages = "1622-1630",
doi = "10.1016/j.jstrokecerebrovasdis.2016.03.011"
}

Kolaković, A., Stanković, A., Đurić, T., Živković, M., Končar, I., Davidović, L., Radak, Đ. J.,& Alavantić, D.. (2016). Gender-Specific Association between Angiotensin II Type 2 Receptor-1332 A/G Gene Polymorphism and Advanced Carotid Atherosclerosis. in Journal of Stroke and Cerebrovascular Diseases, 25(7), 1622-1630.
https://doi.org/10.1016/j.jstrokecerebrovasdis.2016.03.011

Kolaković A, Stanković A, Đurić T, Živković M, Končar I, Davidović L, Radak ĐJ, Alavantić D. Gender-Specific Association between Angiotensin II Type 2 Receptor-1332 A/G Gene Polymorphism and Advanced Carotid Atherosclerosis. in Journal of Stroke and Cerebrovascular Diseases. 2016;25(7):1622-1630.
doi:10.1016/j.jstrokecerebrovasdis.2016.03.011 .

Kolaković, Ana, Stanković, Aleksandra, Đurić, Tamara, Živković, Maja, Končar, Igor, Davidović, Lazar, Radak, Đorđe J., Alavantić, Dragan, "Gender-Specific Association between Angiotensin II Type 2 Receptor-1332 A/G Gene Polymorphism and Advanced Carotid Atherosclerosis" in Journal of Stroke and Cerebrovascular Diseases, 25, no. 7 (2016):1622-1630,
https://doi.org/10.1016/j.jstrokecerebrovasdis.2016.03.011 . .

TY  - JOUR
AU  - Životić, Ivan
AU  - Đurić, Tamara
AU  - Stanković, Aleksandra
AU  - Đorđević, Ana
AU  - Končar, Igor
AU  - Davidović, Lazar
AU  - Alavantić, Dragan
AU  - Živković, Maja
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1126
AB  - Single nucleotide polymorphisms from the chromosome locus 9p21 are reported to carry a risk for various cardiovascular diseases. One of the lead single nucleotide polymorphisms, rs10757278, was mostly investigated in association with coronary artery disease but rarely with carotid atherosclerosis. In this study, we aimed to analyze the association of rs10757278 A/G polymorphism with carotid plaque presence in advanced carotid atherosclerosis. The study included 803 participants, 486 patients with high-grade stenosis ( GT 70%) who were undergoing carotid endarterectomy and 317 controls from Serbian population. Genotypes were determined using the real-time polymerase chain reaction. According to the recessive model of inheritance, GG genotype was significantly and independently associated with carotid plaque in females only (odds ratio 2.42, CI = 1.20-4.90, P = 0.013). Odds ratio was adjusted for age, body mass index, hypertension, TC, LDLC, HDLC and TG, and P value was corrected for multiple comparisons. Our preliminary findings suggest a gender-specific association of rs10757278 polymorphism with carotid plaque. Further studies on larger sample and in genetically and environmentally similar populations are needed.
T2  - Experimental Biology and Medicine
T1  - 9p21 locus rs10757278 is associated with advanced carotid atherosclerosis in a gender-specific manner
VL  - 241
IS  - 11
SP  - 1210
EP  - 1216
DO  - 10.1177/1535370216636718
ER  - 

@article{
author = "Životić, Ivan and Đurić, Tamara and Stanković, Aleksandra and Đorđević, Ana and Končar, Igor and Davidović, Lazar and Alavantić, Dragan and Živković, Maja",
year = "2016",
abstract = "Single nucleotide polymorphisms from the chromosome locus 9p21 are reported to carry a risk for various cardiovascular diseases. One of the lead single nucleotide polymorphisms, rs10757278, was mostly investigated in association with coronary artery disease but rarely with carotid atherosclerosis. In this study, we aimed to analyze the association of rs10757278 A/G polymorphism with carotid plaque presence in advanced carotid atherosclerosis. The study included 803 participants, 486 patients with high-grade stenosis ( GT 70%) who were undergoing carotid endarterectomy and 317 controls from Serbian population. Genotypes were determined using the real-time polymerase chain reaction. According to the recessive model of inheritance, GG genotype was significantly and independently associated with carotid plaque in females only (odds ratio 2.42, CI = 1.20-4.90, P = 0.013). Odds ratio was adjusted for age, body mass index, hypertension, TC, LDLC, HDLC and TG, and P value was corrected for multiple comparisons. Our preliminary findings suggest a gender-specific association of rs10757278 polymorphism with carotid plaque. Further studies on larger sample and in genetically and environmentally similar populations are needed.",
journal = "Experimental Biology and Medicine",
title = "9p21 locus rs10757278 is associated with advanced carotid atherosclerosis in a gender-specific manner",
volume = "241",
number = "11",
pages = "1210-1216",
doi = "10.1177/1535370216636718"
}

Životić, I., Đurić, T., Stanković, A., Đorđević, A., Končar, I., Davidović, L., Alavantić, D.,& Živković, M.. (2016). 9p21 locus rs10757278 is associated with advanced carotid atherosclerosis in a gender-specific manner. in Experimental Biology and Medicine, 241(11), 1210-1216.
https://doi.org/10.1177/1535370216636718

Životić I, Đurić T, Stanković A, Đorđević A, Končar I, Davidović L, Alavantić D, Živković M. 9p21 locus rs10757278 is associated with advanced carotid atherosclerosis in a gender-specific manner. in Experimental Biology and Medicine. 2016;241(11):1210-1216.
doi:10.1177/1535370216636718 .

Životić, Ivan, Đurić, Tamara, Stanković, Aleksandra, Đorđević, Ana, Končar, Igor, Davidović, Lazar, Alavantić, Dragan, Živković, Maja, "9p21 locus rs10757278 is associated with advanced carotid atherosclerosis in a gender-specific manner" in Experimental Biology and Medicine, 241, no. 11 (2016):1210-1216,
https://doi.org/10.1177/1535370216636718 . .

TY  - JOUR
AU  - Bundalo, Maja M.
AU  - Živković, Maja
AU  - Romić, Snježana Đ.
AU  - Tepavčević, Snežana
AU  - Korićanac, Goran
AU  - Đurić, Tamara
AU  - Stanković, Aleksandra
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1132
AB  - Introduction: The cardiovascular renin-angiotensin system (RAS) could be affected by gender and dietary regime. We hypothesized that male rats will be more susceptible to activation of RAS in the heart and aorta, as a response to a fructose-rich diet (FRD). Materials and methods: Both male and female Wistar rats were given a 10% (w/v) fructose solution for 9 weeks. We measured the biochemical parameters, blood pressure (BP) and heart rate. We used Western blot and real-time polymerase chain reaction (PCR) to quantify protein and gene expression. Results: In the male rats, the FRD elevated BP and expression of cardiac angiotensin-converting enzyme (ACE), while the expression of angiotensin-converting enzyme 2 (ACE2) and angiotensin II Type 2 receptor (AT(2)R) were significantly decreased. In female rats, there were no changes in cardiac RAS expression due to FRD. Furthermore, the ACE/AT(1)R axis was overexpressed in the FRD male rats aortae, while only AT(1)R was upregulated in the FRD female rats aortae. ACE2 expression remained unchanged in the aortae of both genders receiving the FRD. Conclusions: The FRD induced gender-specific changes in the expression of the RAS in the heart and aortae of male rats. Further investigations are required in order to get a comprehensive understanding of the underlying mechanisms of gender-specific fructose-induced cardiovascular pathologies.
T2  - Journal of the Renin-Angiotensin-Aldosterone System
T1  - Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta
VL  - 17
IS  - 2
DO  - 10.1177/1470320316642915
ER  - 

@article{
author = "Bundalo, Maja M. and Živković, Maja and Romić, Snježana Đ. and Tepavčević, Snežana and Korićanac, Goran and Đurić, Tamara and Stanković, Aleksandra",
year = "2016",
abstract = "Introduction: The cardiovascular renin-angiotensin system (RAS) could be affected by gender and dietary regime. We hypothesized that male rats will be more susceptible to activation of RAS in the heart and aorta, as a response to a fructose-rich diet (FRD). Materials and methods: Both male and female Wistar rats were given a 10% (w/v) fructose solution for 9 weeks. We measured the biochemical parameters, blood pressure (BP) and heart rate. We used Western blot and real-time polymerase chain reaction (PCR) to quantify protein and gene expression. Results: In the male rats, the FRD elevated BP and expression of cardiac angiotensin-converting enzyme (ACE), while the expression of angiotensin-converting enzyme 2 (ACE2) and angiotensin II Type 2 receptor (AT(2)R) were significantly decreased. In female rats, there were no changes in cardiac RAS expression due to FRD. Furthermore, the ACE/AT(1)R axis was overexpressed in the FRD male rats aortae, while only AT(1)R was upregulated in the FRD female rats aortae. ACE2 expression remained unchanged in the aortae of both genders receiving the FRD. Conclusions: The FRD induced gender-specific changes in the expression of the RAS in the heart and aortae of male rats. Further investigations are required in order to get a comprehensive understanding of the underlying mechanisms of gender-specific fructose-induced cardiovascular pathologies.",
journal = "Journal of the Renin-Angiotensin-Aldosterone System",
title = "Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta",
volume = "17",
number = "2",
doi = "10.1177/1470320316642915"
}

Bundalo, M. M., Živković, M., Romić, S. Đ., Tepavčević, S., Korićanac, G., Đurić, T.,& Stanković, A.. (2016). Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta. in Journal of the Renin-Angiotensin-Aldosterone System, 17(2).
https://doi.org/10.1177/1470320316642915

Bundalo MM, Živković M, Romić SĐ, Tepavčević S, Korićanac G, Đurić T, Stanković A. Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta. in Journal of the Renin-Angiotensin-Aldosterone System. 2016;17(2).
doi:10.1177/1470320316642915 .

Bundalo, Maja M., Živković, Maja, Romić, Snježana Đ., Tepavčević, Snežana, Korićanac, Goran, Đurić, Tamara, Stanković, Aleksandra, "Fructose-rich diet induces gender-specific changes in expression of the renin-angiotensin system in rat heart and upregulates the ACE/AT1R axis in the male rat aorta" in Journal of the Renin-Angiotensin-Aldosterone System, 17, no. 2 (2016),
https://doi.org/10.1177/1470320316642915 . .

TY  - THES
AU  - Bundalo, Maja M.
PY  - 2016
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=3043
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:11284/bdef:Content/download
UR  - http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1025057202
UR  - http://nardus.mpn.gov.rs/123456789/5664
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7279
AB  - Ishrana bogata fruktozom predstavlja bitan faktor u razvoju metaboličkogsindroma koji je povezan sa povećanim rizikom za nastanak kardiovaskularnih bolesti.Smatra se da hronična inflamacija ima bitnu ulogu u njegovoj patogenezi. Ženke suzaštićene od ishranom izazvanih metaboličkih poremećaja i hipertenzije ureproduktivnom periodu. Estrogen, koji utiče na normalno funkcionisanjekardiovaskularnog sistema, bi mogao doprinositi uočenim polno specifičnim razlikama unastanku simptoma metaboličkog sindroma. Proteinske komponente renin-angiotenzinsistema (RAS) imaju bitnu ulogu u nastanku inflamacije, hipertenzije i insulinskerezistencije i na njihovu ekspresiju utiče estradiol. Ova doktorska disertacija je za ciljimala da ispita da li pol i estradiol doprinose promenama u ekspresiji komponenti RAS-a[angiotenzin konvertujućeg enzima (ACE), angiotenzin konvertujućeg enzima 2 (ACE2),angiotenzinskog receptora tipa 1 (AT1R), angiotenzinskog receptora tipa 2 (AT2R) ikolektrina] i medijatora inflamacije i remodelovanja tkiva srca [nuklearnog faktora κB(NFκB), matriks metaloproteinaze-9 (MMP-9) i liganda 16 iz familije hemokina CXC(CXCL16)] kod animalnog modela metaboličkog sindroma.Mužjaci i ženke pacova koji su pili 10% rastvor fruktoze umesto vode u trajanjuod 9 nedelja predstavljali su animalni model metaboličkog sindroma korišćen u ovojstudiji. Radi ispitivanja efekata estradiola jedan deo ženki pacova je ovarijektomisan ipodeljen u tri grupe pri čemi je jedna grupa pored standardne laboratorijske hrane pilavodu, druga grupa je pila 10% rastvor fruktoze, a treća grupa je pored rasvora fruktozeprimala i supstitucionu terapiju estradiolom. Ishrana bogata fruktozom je uzrokovalapovećanje krvnog pritiska samo kod mužjaka pacova. Ovaj tip ishrane nije doveo dopromena u masi srca niti u odnosu masa srca/masa tela ni kod jednog pola, kao ni kodovarijektomisanih životinja što ukazuje da se hipertrofija srca nije razvila...
AB  - Fructose rich diet (FRD) represents an important factor in the development ofmetabolic syndrome. Metabolic syndrome is associated with increased risk forcardiovascular diseases occurrence and chronic inflammation has a major role in itspathogenesis. Females are protected from diet-induced metabolic disturbances andhypertension in their reproductive period. Estrogen, which influences the cardiovascularsystem, could contribute to the observed gender-specific differences in the onset ofmetabolic syndrome. Components of the renin-angiotensin system (RAS), the synthesisof which is mediated by estrogen, have an important role in the inflammatory processes,hypertension and insulin resistance. Almost all of the components of metabolic syndromeincrease the activity of RAS, which finally results in increased oxidative stress andinflammation. The aim of this doctoral dissertation was to investigate sex specific changesand role of estradiol in the expression of RAS components [angiotensin convertingenzyme (ACE), angiotensin converting enzyme 2 (ACE2), angiotensin receptor type 1(AT1R), angiotensin receptor type 2 (AT2R) and collectrin], as well as mediators ofinflammation and remodeling of heart tissue [nuclear faktor κB (NFκB), matrixmetalloproteinse-9 (MMP-9) and CXCL16 chemokine] in the animal model of metabolicsyndrome.Male and female rats, which consumed 10% fructose solution instead of water for9 weeks, represent an animal model of metabolic syndrome that was used in this study. Inorder to examine the effects of estradiol in the context of FRD, female rats wereovariectomized and divided in three groups: fed normal diet, fed FRD, and fed FRD andsubjected to estradiol replacement therapy. FRD increased blood pressure only in malerats. This diet regime didn't cause heart hypertrophy neither in intact males and females,nor in ovariectomized females...
PB  - Универзитет у Београду, Биолошки факултет
T2  - Универзитет у Београду
T1  - Uticaj ishrane bogate fruktozom na ekspresiju komponenti renin-angiotenzin sistema i inflamacije u tkivu srca pacova: polno specifične razlike
T1  - The effect of fructose rich diet on the expression of renin-angiostensin system components and inflamatory molecules in the rat heart: sex specific differences
UR  - https://hdl.handle.net/21.15107/rcub_nardus_5664
ER  - 

@phdthesis{
author = "Bundalo, Maja M.",
year = "2016",
abstract = "Ishrana bogata fruktozom predstavlja bitan faktor u razvoju metaboličkogsindroma koji je povezan sa povećanim rizikom za nastanak kardiovaskularnih bolesti.Smatra se da hronična inflamacija ima bitnu ulogu u njegovoj patogenezi. Ženke suzaštićene od ishranom izazvanih metaboličkih poremećaja i hipertenzije ureproduktivnom periodu. Estrogen, koji utiče na normalno funkcionisanjekardiovaskularnog sistema, bi mogao doprinositi uočenim polno specifičnim razlikama unastanku simptoma metaboličkog sindroma. Proteinske komponente renin-angiotenzinsistema (RAS) imaju bitnu ulogu u nastanku inflamacije, hipertenzije i insulinskerezistencije i na njihovu ekspresiju utiče estradiol. Ova doktorska disertacija je za ciljimala da ispita da li pol i estradiol doprinose promenama u ekspresiji komponenti RAS-a[angiotenzin konvertujućeg enzima (ACE), angiotenzin konvertujućeg enzima 2 (ACE2),angiotenzinskog receptora tipa 1 (AT1R), angiotenzinskog receptora tipa 2 (AT2R) ikolektrina] i medijatora inflamacije i remodelovanja tkiva srca [nuklearnog faktora κB(NFκB), matriks metaloproteinaze-9 (MMP-9) i liganda 16 iz familije hemokina CXC(CXCL16)] kod animalnog modela metaboličkog sindroma.Mužjaci i ženke pacova koji su pili 10% rastvor fruktoze umesto vode u trajanjuod 9 nedelja predstavljali su animalni model metaboličkog sindroma korišćen u ovojstudiji. Radi ispitivanja efekata estradiola jedan deo ženki pacova je ovarijektomisan ipodeljen u tri grupe pri čemi je jedna grupa pored standardne laboratorijske hrane pilavodu, druga grupa je pila 10% rastvor fruktoze, a treća grupa je pored rasvora fruktozeprimala i supstitucionu terapiju estradiolom. Ishrana bogata fruktozom je uzrokovalapovećanje krvnog pritiska samo kod mužjaka pacova. Ovaj tip ishrane nije doveo dopromena u masi srca niti u odnosu masa srca/masa tela ni kod jednog pola, kao ni kodovarijektomisanih životinja što ukazuje da se hipertrofija srca nije razvila..., Fructose rich diet (FRD) represents an important factor in the development ofmetabolic syndrome. Metabolic syndrome is associated with increased risk forcardiovascular diseases occurrence and chronic inflammation has a major role in itspathogenesis. Females are protected from diet-induced metabolic disturbances andhypertension in their reproductive period. Estrogen, which influences the cardiovascularsystem, could contribute to the observed gender-specific differences in the onset ofmetabolic syndrome. Components of the renin-angiotensin system (RAS), the synthesisof which is mediated by estrogen, have an important role in the inflammatory processes,hypertension and insulin resistance. Almost all of the components of metabolic syndromeincrease the activity of RAS, which finally results in increased oxidative stress andinflammation. The aim of this doctoral dissertation was to investigate sex specific changesand role of estradiol in the expression of RAS components [angiotensin convertingenzyme (ACE), angiotensin converting enzyme 2 (ACE2), angiotensin receptor type 1(AT1R), angiotensin receptor type 2 (AT2R) and collectrin], as well as mediators ofinflammation and remodeling of heart tissue [nuclear faktor κB (NFκB), matrixmetalloproteinse-9 (MMP-9) and CXCL16 chemokine] in the animal model of metabolicsyndrome.Male and female rats, which consumed 10% fructose solution instead of water for9 weeks, represent an animal model of metabolic syndrome that was used in this study. Inorder to examine the effects of estradiol in the context of FRD, female rats wereovariectomized and divided in three groups: fed normal diet, fed FRD, and fed FRD andsubjected to estradiol replacement therapy. FRD increased blood pressure only in malerats. This diet regime didn't cause heart hypertrophy neither in intact males and females,nor in ovariectomized females...",
publisher = "Универзитет у Београду, Биолошки факултет",
journal = "Универзитет у Београду",
title = "Uticaj ishrane bogate fruktozom na ekspresiju komponenti renin-angiotenzin sistema i inflamacije u tkivu srca pacova: polno specifične razlike, The effect of fructose rich diet on the expression of renin-angiostensin system components and inflamatory molecules in the rat heart: sex specific differences",
url = "https://hdl.handle.net/21.15107/rcub_nardus_5664"
}

Bundalo, M. M.. (2016). Uticaj ishrane bogate fruktozom na ekspresiju komponenti renin-angiotenzin sistema i inflamacije u tkivu srca pacova: polno specifične razlike. in Универзитет у Београду
Универзитет у Београду, Биолошки факултет..
https://hdl.handle.net/21.15107/rcub_nardus_5664

Bundalo MM. Uticaj ishrane bogate fruktozom na ekspresiju komponenti renin-angiotenzin sistema i inflamacije u tkivu srca pacova: polno specifične razlike. in Универзитет у Београду. 2016;.
https://hdl.handle.net/21.15107/rcub_nardus_5664 .

Bundalo, Maja M., "Uticaj ishrane bogate fruktozom na ekspresiju komponenti renin-angiotenzin sistema i inflamacije u tkivu srca pacova: polno specifične razlike" in Универзитет у Београду (2016),
https://hdl.handle.net/21.15107/rcub_nardus_5664 .

TY  - JOUR
AU  - Jovanović, Ivan G.
AU  - Živković, Maja
AU  - Kostić, Mirjana M.
AU  - Krstić, Zoran
AU  - Đurić, Tamara
AU  - Kolić, Ivana
AU  - Alavantić, Dragan
AU  - Stanković, Aleksandra
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1182
AB  - Background: The genetic cause of most congenital anomalies of the kidney and urinary tract (CAKUT) cases remains unknown, therefore the novel approaches in searching for the common disease denominators are required. miRs regulate gene expression in humans and therefore have potentially therapeutic and biomarker properties. No studies thus far have attempted to explore the miRs in human CAKUT. We applied a new strategy to identify most specific miRs associated with CAKUT, in pediatric patients. Methods: Data from the whole genome expression, gathered from ureter tissue samples of 19 patients and 7 controls, were used for the bioinformatic prediction of miRs activity in CAKUT. We integrated microarray gene expression data and miR target predictions from multiple prediction algorithms using Co-inertia analysis (CIA) in conjunction with correspondence analysis and between group analysis, to produce a ranked list of miRs associated with CAKUT. The CIA included five different sequence based miR target prediction algorithms and the Co-expression Meta-analysis of miR Targets. For the experimental validation of expression of miRs identified by the CIA we used tissue from 36 CAKUT patients and 9 controls. The results of gene ontology (GO) analysis on co-expressed targets of miRs associated with CAKUT were used for the selection of putative biological processes relevant to CAKUT. Results: We identified 7 miRs with a potential role in CAKUT. The top ranked miRs from miRCos communities 4, 1 and 7 were chosen for experimental validation of expression in CAKUT tissue. The 5.7 fold increase of hsa-miR-144 expression in human tissue from CAKUT patients compared to controls (p = 0.005) was observed. From the GO we selected 7 biological processes that could contribute to CAKUT, which genes are potentially influenced by hsa-miR-144. The hsa-miR-200a, hsa-miR-183 and hsa-miR-375 werent differentially expressed in CAKUT. Conclusions: This study shows that integrative approach applied here was useful in identification of the miRs associated with CAKUT. The hsa-miR-144, first time identified in CAKUT, could be connected with biological processes crucial for normal development of kidney and urinary tract. Further functional analysis must follow to reveal the impact of hsa-miR-144 on CAKUT occurrence.
T2  - Journal of Translational Medicine
T1  - Transcriptome-wide based identification of miRs in congenital anomalies of the kidney and urinary tract (CAKUT) in children: the significant upregulation of tissue miR-144 expression
VL  - 14
IS  - 1
SP  - 193
DO  - 10.1186/s12967-016-0955-0
ER  - 

@article{
author = "Jovanović, Ivan G. and Živković, Maja and Kostić, Mirjana M. and Krstić, Zoran and Đurić, Tamara and Kolić, Ivana and Alavantić, Dragan and Stanković, Aleksandra",
year = "2016",
abstract = "Background: The genetic cause of most congenital anomalies of the kidney and urinary tract (CAKUT) cases remains unknown, therefore the novel approaches in searching for the common disease denominators are required. miRs regulate gene expression in humans and therefore have potentially therapeutic and biomarker properties. No studies thus far have attempted to explore the miRs in human CAKUT. We applied a new strategy to identify most specific miRs associated with CAKUT, in pediatric patients. Methods: Data from the whole genome expression, gathered from ureter tissue samples of 19 patients and 7 controls, were used for the bioinformatic prediction of miRs activity in CAKUT. We integrated microarray gene expression data and miR target predictions from multiple prediction algorithms using Co-inertia analysis (CIA) in conjunction with correspondence analysis and between group analysis, to produce a ranked list of miRs associated with CAKUT. The CIA included five different sequence based miR target prediction algorithms and the Co-expression Meta-analysis of miR Targets. For the experimental validation of expression of miRs identified by the CIA we used tissue from 36 CAKUT patients and 9 controls. The results of gene ontology (GO) analysis on co-expressed targets of miRs associated with CAKUT were used for the selection of putative biological processes relevant to CAKUT. Results: We identified 7 miRs with a potential role in CAKUT. The top ranked miRs from miRCos communities 4, 1 and 7 were chosen for experimental validation of expression in CAKUT tissue. The 5.7 fold increase of hsa-miR-144 expression in human tissue from CAKUT patients compared to controls (p = 0.005) was observed. From the GO we selected 7 biological processes that could contribute to CAKUT, which genes are potentially influenced by hsa-miR-144. The hsa-miR-200a, hsa-miR-183 and hsa-miR-375 werent differentially expressed in CAKUT. Conclusions: This study shows that integrative approach applied here was useful in identification of the miRs associated with CAKUT. The hsa-miR-144, first time identified in CAKUT, could be connected with biological processes crucial for normal development of kidney and urinary tract. Further functional analysis must follow to reveal the impact of hsa-miR-144 on CAKUT occurrence.",
journal = "Journal of Translational Medicine",
title = "Transcriptome-wide based identification of miRs in congenital anomalies of the kidney and urinary tract (CAKUT) in children: the significant upregulation of tissue miR-144 expression",
volume = "14",
number = "1",
pages = "193",
doi = "10.1186/s12967-016-0955-0"
}

Jovanović, I. G., Živković, M., Kostić, M. M., Krstić, Z., Đurić, T., Kolić, I., Alavantić, D.,& Stanković, A.. (2016). Transcriptome-wide based identification of miRs in congenital anomalies of the kidney and urinary tract (CAKUT) in children: the significant upregulation of tissue miR-144 expression. in Journal of Translational Medicine, 14(1), 193.
https://doi.org/10.1186/s12967-016-0955-0

Jovanović IG, Živković M, Kostić MM, Krstić Z, Đurić T, Kolić I, Alavantić D, Stanković A. Transcriptome-wide based identification of miRs in congenital anomalies of the kidney and urinary tract (CAKUT) in children: the significant upregulation of tissue miR-144 expression. in Journal of Translational Medicine. 2016;14(1):193.
doi:10.1186/s12967-016-0955-0 .

Jovanović, Ivan G., Živković, Maja, Kostić, Mirjana M., Krstić, Zoran, Đurić, Tamara, Kolić, Ivana, Alavantić, Dragan, Stanković, Aleksandra, "Transcriptome-wide based identification of miRs in congenital anomalies of the kidney and urinary tract (CAKUT) in children: the significant upregulation of tissue miR-144 expression" in Journal of Translational Medicine, 14, no. 1 (2016):193,
https://doi.org/10.1186/s12967-016-0955-0 . .

TY  - THES
AU  - Jovanović, Ivan G.
PY  - 2016
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=4808
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:15112/bdef:Content/download
UR  - http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1025149106
UR  - http://nardus.mpn.gov.rs/123456789/7884
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7316
AB  - Urođene anomalije bubrega i urinarnog trakta (engl. Congenital Anomalies of the Kidney and Urinary Tract – CAKUT) su razlog nastanka čak polovine slučajeva terminalne bubrežne insuficijencije ali patofiziološka osnova ove bolesti još uvek nije poznata u potpunosti pa je samim tim otežana prevencija i terapija. U ovoj studiji je, upoređivanjem ekspresije celokupnog genoma u tkivu uretera pacijenata sa CAKUT-om i zdravih kontrola, identifikovano 78 diferencijalno eksprimiranih gena. Bioinformatičkom analizom je po prvi put zaključeno da postoji visok nivo kompleksnosti bioloških procesa i molekularnih puteva u tkivu čoveka koji su u CAKUT-u diferencijalno regulisani i čije važne interakcije se mogu predstaviti sa sedam molekularnih mreža, od kojih četiri sadrže gene sa funkcijama koje se direktno mogu asocirati sa CAKUT-om. Eksperimentalnom validacijom ključnih mreža qRT-PCR metodom utvrđen je povišen nivo iRNK za gene LCN2 (7,6 puta), PROM1 (8 puta) i SOSTDC1 (5,6 puta) i snižen nivo iRNK za gene RASD1 (4,5 puta), INA (3,3 puta) i TAC3 (6,6 puta) u tkivu uretera pacijenata u poređenju sa kontrolnim tkivom, koji mogu biti molekularni markeri za CAKUT. Ove mreže su ujedno i prikaz interakcija ključnih molekula u CAKUT-u i predstavljaju temelj budućih funkcionalnih studija. Primenom metode koja povezuje podatke sa genskog ekspresionog čipa i predikcije vezujućih mesta različitih miRNK iz više predikcionih algoritama, sa unapređenom rezolucijom, identifikovane su miRNK sa potencijalno povišenom ekspresijom u CAKUT-u u odnosu na zdrave kontrole. Validacijom ključnih miRNK qRT-PCR metodom je identifikovan povišen nivo miR-144 (5,7 puta) u tkivu uretera pacijenata u odnosu na kontrole, koji može biti molekularni marker za CAKUT.
AB  - Congenital anomalies of the kidney and urinary tract (CAKUT) are the cause for half of the cases with renal failure, but pathophysiological basis of this disease is not fully known. Therefore, the therapy and prevention of the disease is difficult. In this study, by comparing the whole-genome expression in the ureter tissue of patients with CAKUT and healthy controls, 78 differentially expressed genes were identified. By employing bioinformatical analysis it was concluded that there is a high level of complexity of biological processes and molecular pathways, differentialy regulated in CAKUT, whose important interactions can be represented with seven molecular networks, of which four contain genes with functions that can be directly associated with CAKUT. Experimental validation of key networks by qRT-PCR method identified elevated mRNA levels of LCN2 (7.6 fold), PROM1 (8 fold) and SOSTDC1 (5.6 fold), and decreased mRNA levels of RASD1 (4.5 fold), INA (3.3 fold) and TAC3 (6.6 fold) in the ureter tissue of the patients compared to control tissue, which may be molecular markers for CAKUT. These networks display the interactions of key molecules in CAKUT and provide the basis for future functional studies, as well. By applying the method that links microarray gene expression data and prediction of miRNA binding sites from several prediction algorithms, with enhanced resolution, miRNAs with potentialy upregulated expression in CAKUT compared to healthy controls were identified. Validation of key miRNAs by qRT-PCR method identified increased level of miR-144 (5.7 fold) in the ureter tissue of the patients compared to controls, which may be a molecular marker for CAKUT.
PB  - Универзитет у Београду, Биолошки факултет
T2  - Универзитет у Београду
T1  - Analiza ekspresije celokupnog genoma u cilju identifikacije ključnih gena i mikroRNK za nastanak urođenih anomalija bubrega i urinarnog trakta čoveka
UR  - https://hdl.handle.net/21.15107/rcub_nardus_7884
ER  - 

@phdthesis{
author = "Jovanović, Ivan G.",
year = "2016",
abstract = "Urođene anomalije bubrega i urinarnog trakta (engl. Congenital Anomalies of the Kidney and Urinary Tract – CAKUT) su razlog nastanka čak polovine slučajeva terminalne bubrežne insuficijencije ali patofiziološka osnova ove bolesti još uvek nije poznata u potpunosti pa je samim tim otežana prevencija i terapija. U ovoj studiji je, upoređivanjem ekspresije celokupnog genoma u tkivu uretera pacijenata sa CAKUT-om i zdravih kontrola, identifikovano 78 diferencijalno eksprimiranih gena. Bioinformatičkom analizom je po prvi put zaključeno da postoji visok nivo kompleksnosti bioloških procesa i molekularnih puteva u tkivu čoveka koji su u CAKUT-u diferencijalno regulisani i čije važne interakcije se mogu predstaviti sa sedam molekularnih mreža, od kojih četiri sadrže gene sa funkcijama koje se direktno mogu asocirati sa CAKUT-om. Eksperimentalnom validacijom ključnih mreža qRT-PCR metodom utvrđen je povišen nivo iRNK za gene LCN2 (7,6 puta), PROM1 (8 puta) i SOSTDC1 (5,6 puta) i snižen nivo iRNK za gene RASD1 (4,5 puta), INA (3,3 puta) i TAC3 (6,6 puta) u tkivu uretera pacijenata u poređenju sa kontrolnim tkivom, koji mogu biti molekularni markeri za CAKUT. Ove mreže su ujedno i prikaz interakcija ključnih molekula u CAKUT-u i predstavljaju temelj budućih funkcionalnih studija. Primenom metode koja povezuje podatke sa genskog ekspresionog čipa i predikcije vezujućih mesta različitih miRNK iz više predikcionih algoritama, sa unapređenom rezolucijom, identifikovane su miRNK sa potencijalno povišenom ekspresijom u CAKUT-u u odnosu na zdrave kontrole. Validacijom ključnih miRNK qRT-PCR metodom je identifikovan povišen nivo miR-144 (5,7 puta) u tkivu uretera pacijenata u odnosu na kontrole, koji može biti molekularni marker za CAKUT., Congenital anomalies of the kidney and urinary tract (CAKUT) are the cause for half of the cases with renal failure, but pathophysiological basis of this disease is not fully known. Therefore, the therapy and prevention of the disease is difficult. In this study, by comparing the whole-genome expression in the ureter tissue of patients with CAKUT and healthy controls, 78 differentially expressed genes were identified. By employing bioinformatical analysis it was concluded that there is a high level of complexity of biological processes and molecular pathways, differentialy regulated in CAKUT, whose important interactions can be represented with seven molecular networks, of which four contain genes with functions that can be directly associated with CAKUT. Experimental validation of key networks by qRT-PCR method identified elevated mRNA levels of LCN2 (7.6 fold), PROM1 (8 fold) and SOSTDC1 (5.6 fold), and decreased mRNA levels of RASD1 (4.5 fold), INA (3.3 fold) and TAC3 (6.6 fold) in the ureter tissue of the patients compared to control tissue, which may be molecular markers for CAKUT. These networks display the interactions of key molecules in CAKUT and provide the basis for future functional studies, as well. By applying the method that links microarray gene expression data and prediction of miRNA binding sites from several prediction algorithms, with enhanced resolution, miRNAs with potentialy upregulated expression in CAKUT compared to healthy controls were identified. Validation of key miRNAs by qRT-PCR method identified increased level of miR-144 (5.7 fold) in the ureter tissue of the patients compared to controls, which may be a molecular marker for CAKUT.",
publisher = "Универзитет у Београду, Биолошки факултет",
journal = "Универзитет у Београду",
title = "Analiza ekspresije celokupnog genoma u cilju identifikacije ključnih gena i mikroRNK za nastanak urođenih anomalija bubrega i urinarnog trakta čoveka",
url = "https://hdl.handle.net/21.15107/rcub_nardus_7884"
}

Jovanović, I. G.. (2016). Analiza ekspresije celokupnog genoma u cilju identifikacije ključnih gena i mikroRNK za nastanak urođenih anomalija bubrega i urinarnog trakta čoveka. in Универзитет у Београду
Универзитет у Београду, Биолошки факултет..
https://hdl.handle.net/21.15107/rcub_nardus_7884

Jovanović IG. Analiza ekspresije celokupnog genoma u cilju identifikacije ključnih gena i mikroRNK za nastanak urođenih anomalija bubrega i urinarnog trakta čoveka. in Универзитет у Београду. 2016;.
https://hdl.handle.net/21.15107/rcub_nardus_7884 .

Jovanović, Ivan G., "Analiza ekspresije celokupnog genoma u cilju identifikacije ključnih gena i mikroRNK za nastanak urođenih anomalija bubrega i urinarnog trakta čoveka" in Универзитет у Београду (2016),
https://hdl.handle.net/21.15107/rcub_nardus_7884 .

TY  - JOUR
AU  - Bundalo, Maja M.
AU  - Živković, Maja
AU  - Tepavčević, Snežana
AU  - Ćulafić, Tijana
AU  - Korićanac, Goran
AU  - Stanković, Aleksandra
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/570
AB  - The renin-angiotensin system has been implicated in the development of metabolic syndrome and appears to be a key in the local tissue control of normal cardiac functions. Physiological concentrations of estrogens have been shown to be cardioprotective, especially against the damaging effects of fructose-rich diet. The aim of the study was to investigate the expression of the renin-angiotensin system molecules with potentially deleterious effect on the heart (angiotensin-converting enzyme and angiotensin II type 1 receptor) and those with potentially protective effects, (angiotensin-converting enzyme 2 and angiotensin II type 2 receptor), in ovariectomized fructose fed female rats with 17-estradiol replacement. Real-time PCR and Western blot analysis were used for quantification of gene and protein expression in the heart. Fructose diet increased the expression of angiotensin-converting enzyme and angiotensin II type 1 receptor and decreased the expression of angiotensin-converting enzyme 2 and angiotensin II type 2 receptor. On the other hand, estradiol replacement seems to undo fructose diet effects on cardiac renin-angiotensin system. Downregulation of angiotensin-converting enzyme and angiotensin II type 1 receptor, and reversion of expression of both potentially protective molecules, angiotensin-converting enzyme 2 and angiotensin II type 2 receptor, to the control level in cardiac tissue took place. Obtained results suggest that estradiol may reverse the harmful effect of fructose-rich diet on the expression of renin-angiotensin system molecules. These findings may also be important in further research of phenotypes like insulin resistance, metabolic syndrome, and following cardiovascular pathology in females.
T2  - Hormone and Metabolic Research
T1  - Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol
VL  - 47
IS  - 7
SP  - 521
EP  - 527
DO  - 10.1055/s-0034-1394373
ER  - 

@article{
author = "Bundalo, Maja M. and Živković, Maja and Tepavčević, Snežana and Ćulafić, Tijana and Korićanac, Goran and Stanković, Aleksandra",
year = "2015",
abstract = "The renin-angiotensin system has been implicated in the development of metabolic syndrome and appears to be a key in the local tissue control of normal cardiac functions. Physiological concentrations of estrogens have been shown to be cardioprotective, especially against the damaging effects of fructose-rich diet. The aim of the study was to investigate the expression of the renin-angiotensin system molecules with potentially deleterious effect on the heart (angiotensin-converting enzyme and angiotensin II type 1 receptor) and those with potentially protective effects, (angiotensin-converting enzyme 2 and angiotensin II type 2 receptor), in ovariectomized fructose fed female rats with 17-estradiol replacement. Real-time PCR and Western blot analysis were used for quantification of gene and protein expression in the heart. Fructose diet increased the expression of angiotensin-converting enzyme and angiotensin II type 1 receptor and decreased the expression of angiotensin-converting enzyme 2 and angiotensin II type 2 receptor. On the other hand, estradiol replacement seems to undo fructose diet effects on cardiac renin-angiotensin system. Downregulation of angiotensin-converting enzyme and angiotensin II type 1 receptor, and reversion of expression of both potentially protective molecules, angiotensin-converting enzyme 2 and angiotensin II type 2 receptor, to the control level in cardiac tissue took place. Obtained results suggest that estradiol may reverse the harmful effect of fructose-rich diet on the expression of renin-angiotensin system molecules. These findings may also be important in further research of phenotypes like insulin resistance, metabolic syndrome, and following cardiovascular pathology in females.",
journal = "Hormone and Metabolic Research",
title = "Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol",
volume = "47",
number = "7",
pages = "521-527",
doi = "10.1055/s-0034-1394373"
}

Bundalo, M. M., Živković, M., Tepavčević, S., Ćulafić, T., Korićanac, G.,& Stanković, A.. (2015). Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol. in Hormone and Metabolic Research, 47(7), 521-527.
https://doi.org/10.1055/s-0034-1394373

Bundalo MM, Živković M, Tepavčević S, Ćulafić T, Korićanac G, Stanković A. Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol. in Hormone and Metabolic Research. 2015;47(7):521-527.
doi:10.1055/s-0034-1394373 .

Bundalo, Maja M., Živković, Maja, Tepavčević, Snežana, Ćulafić, Tijana, Korićanac, Goran, Stanković, Aleksandra, "Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol" in Hormone and Metabolic Research, 47, no. 7 (2015):521-527,
https://doi.org/10.1055/s-0034-1394373 . .

TY  - JOUR
AU  - Bundalo, Maja M.
AU  - Živković, Maja
AU  - Ćulafić, Tijana
AU  - Stojiljković, Mojca D.
AU  - Korićanac, Goran
AU  - Stanković, Aleksandra
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1112
AB  - Fructose-rich diet induces metabolic changes similar to those observed in metabolic syndrome. Among other matrix metalloproteinases, MMP-9 has an important role in adverse cardiac remodelling and might have a role in the development of cardiovascular disorders associated with metabolic syndrome. The changes of MMP-9 expression could be mediated via the NF kappa B pathway. In this study we investigated the effect of fructose-rich diet on MMP-9 expression in the heart of male and female rats, along with the effect of fructose-rich diet and oestradiol on MMP-9 expression in ovariectomized females. We further assessed the effect of fructose-rich diet and oestradiol on NF kappa B activation, measured as the level of p65 phosphorylation at Ser 276. The results showed that the diet regime did not affect the heart mass. Higher MMP-9 gene expression was found in cardiac tissue of male rats fed the fructose-rich diet than in females on the same diet regime. In ovariectomized females, fructose-rich diet upregulated MMP-9 protein and mRNA expression in the heart, as well as phosphorylation of the p65 subunit of NF kappa B at Ser 276. Oestradiol replacement therapy reverted these changes in the heart of ovariectomized females. This study has shown that oestradiol could revert the early molecular changes in MMP-9 expression induced by fructose-rich diet that occurred before cardiac hypertrophy development by decreasing phosphorylation of the NF kappa B p65 subunit at Ser 276.
T2  - Folia Biologica
T1  - Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation
VL  - 61
IS  - 6
SP  - 233
EP  - 240
UR  - https://hdl.handle.net/21.15107/rcub_vinar_1112
ER  - 

@article{
author = "Bundalo, Maja M. and Živković, Maja and Ćulafić, Tijana and Stojiljković, Mojca D. and Korićanac, Goran and Stanković, Aleksandra",
year = "2015",
abstract = "Fructose-rich diet induces metabolic changes similar to those observed in metabolic syndrome. Among other matrix metalloproteinases, MMP-9 has an important role in adverse cardiac remodelling and might have a role in the development of cardiovascular disorders associated with metabolic syndrome. The changes of MMP-9 expression could be mediated via the NF kappa B pathway. In this study we investigated the effect of fructose-rich diet on MMP-9 expression in the heart of male and female rats, along with the effect of fructose-rich diet and oestradiol on MMP-9 expression in ovariectomized females. We further assessed the effect of fructose-rich diet and oestradiol on NF kappa B activation, measured as the level of p65 phosphorylation at Ser 276. The results showed that the diet regime did not affect the heart mass. Higher MMP-9 gene expression was found in cardiac tissue of male rats fed the fructose-rich diet than in females on the same diet regime. In ovariectomized females, fructose-rich diet upregulated MMP-9 protein and mRNA expression in the heart, as well as phosphorylation of the p65 subunit of NF kappa B at Ser 276. Oestradiol replacement therapy reverted these changes in the heart of ovariectomized females. This study has shown that oestradiol could revert the early molecular changes in MMP-9 expression induced by fructose-rich diet that occurred before cardiac hypertrophy development by decreasing phosphorylation of the NF kappa B p65 subunit at Ser 276.",
journal = "Folia Biologica",
title = "Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation",
volume = "61",
number = "6",
pages = "233-240",
url = "https://hdl.handle.net/21.15107/rcub_vinar_1112"
}

Bundalo, M. M., Živković, M., Ćulafić, T., Stojiljković, M. D., Korićanac, G.,& Stanković, A.. (2015). Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation. in Folia Biologica, 61(6), 233-240.
https://hdl.handle.net/21.15107/rcub_vinar_1112

Bundalo MM, Živković M, Ćulafić T, Stojiljković MD, Korićanac G, Stanković A. Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation. in Folia Biologica. 2015;61(6):233-240.
https://hdl.handle.net/21.15107/rcub_vinar_1112 .

Bundalo, Maja M., Živković, Maja, Ćulafić, Tijana, Stojiljković, Mojca D., Korićanac, Goran, Stanković, Aleksandra, "Oestradiol Treatment Counteracts the Effect of Fructose-Rich Diet on Matrix Metalloproteinase 9 Expression and NF kappa B Activation" in Folia Biologica, 61, no. 6 (2015):233-240,
https://hdl.handle.net/21.15107/rcub_vinar_1112 .