Đorđević, Ana D.

Link to this page

Authority KeyName Variants
orcid::0000-0002-7042-1631
  • Đorđević, Ana D. (34)
Projects
Role of steroid hormones in neuroendocrine adaptation to stress and pathophysiology of metabolic syndrome - molecular mechanisms and clinical implications Defining a cluster of molecular biomarkers for improved diagnostics and therapy of mood disorders
Genetic basis of human vascular and inflammatory diseases An integral study to identify the regional genetic and environmental risk factors for the common noncommunicable diseases in the human population of Serbia - INGEMA_S
Ministry of Science and Technological Development of the Republic of Serbia [143042B] Hormonal regulation of expression and activity of the nitric oxide synthase and sodium-potassium pump in experimental models of insulin resistance, diabetes and cardiovascular disorders
Molecular mechanisms of cellular responses on pathological changes in central neuronal system and peripheral organs of mammals Modulation of intracellular energy balance-controlling signalling pathways in therapy of cancer and neuro-immuno-endocrine disorders
Molecular genetic and ecophysiological researches on the protection of autochthonous animal genetic resources, sustaining domestic animals’ welfare, health and reproduction, and safe food production Ministry of Science and Technological Development of Serbia [143042B]
Ministry of Science of Serbia [14304213] Ministry of Science of the Republic of Serbia [143003, 143042B]
Ministry of Science of the Republic of Serbia [143042B, 43003] Ministry of Science of the Republic of Serbia [143044B]
Ministry of Sciences of Serbia [143042B], Wellcome Trust [069024] Ministry of Sciences of the Republic of Serbia [ON143042B]
Wellcome Trust [069024], Ministry of Sciences of Serbia [ON14304213]

Author's Bibliography

Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue

Bundalo, Maja M.; Đorđević, Ana D.; Bursac, Biljana; Živković, Maja; Korićanac, Goran; Stanković, Aleksandra

(2017)

TY  - JOUR
AU  - Bundalo, Maja M.
AU  - Đorđević, Ana D.
AU  - Bursac, Biljana
AU  - Živković, Maja
AU  - Korićanac, Goran
AU  - Stanković, Aleksandra
PY  - 2017
UR  - http://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 Bursac, Biljana and Živković, Maja and Korićanac, Goran and Stanković, Aleksandra",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1839",
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., Bursac, 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.
Applied Physiology Nutrition and Metabolism, 42(12), 1254-1263.
https://doi.org/10.1139/apnm-2016-0725
Bundalo MM, Đorđević AD, Bursac 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. Applied Physiology Nutrition and Metabolism. 2017;42(12):1254-1263
Bundalo Maja M., Đorđević Ana D., Bursac 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" Applied Physiology Nutrition and Metabolism, 42, no. 12 (2017):1254-1263,
https://doi.org/10.1139/apnm-2016-0725 .
1
3
3
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Snps in the Vicinity of Lgals-3 Locus and Different Shape-Types of Heart Remodeling After the First Myocardial Infarction: Preliminary Results

Đorđević, Ana D.; Živković, Maja; Dekleva, Milica; Marković-Nikolić, Nataša; Alavantić, Dragan; Stanković, Aleksandra; Đurić, Tamara

(2017)

TY  - CONF
AU  - Đorđević, Ana D.
AU  - Živković, Maja
AU  - Dekleva, Milica
AU  - Marković-Nikolić, Nataša
AU  - Alavantić, Dragan
AU  - Stanković, Aleksandra
AU  - Đurić, Tamara
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7177
C3  - Atherosclerosis
T1  - Snps in the Vicinity of Lgals-3 Locus and Different Shape-Types of Heart Remodeling After the First Myocardial Infarction: Preliminary Results
VL  - 263
SP  - E180
EP  - E180
DO  - 10.1016/j.atherosclerosis.2017.06.578
ER  - 
@conference{
author = "Đorđević, Ana D. and Živković, Maja and Dekleva, Milica and Marković-Nikolić, Nataša and Alavantić, Dragan and Stanković, Aleksandra and Đurić, Tamara",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/7177",
journal = "Atherosclerosis",
title = "Snps in the Vicinity of Lgals-3 Locus and Different Shape-Types of Heart Remodeling After the First Myocardial Infarction: Preliminary Results",
volume = "263",
pages = "E180-E180",
doi = "10.1016/j.atherosclerosis.2017.06.578"
}
Đorđević, A. D., Živković, M., Dekleva, M., Marković-Nikolić, N., Alavantić, D., Stanković, A.,& Đurić, T. (2017). Snps in the Vicinity of Lgals-3 Locus and Different Shape-Types of Heart Remodeling After the First Myocardial Infarction: Preliminary Results.
Atherosclerosis, 263, E180-E180.
https://doi.org/10.1016/j.atherosclerosis.2017.06.578
Đorđević AD, Živković M, Dekleva M, Marković-Nikolić N, Alavantić D, Stanković A, Đurić T. Snps in the Vicinity of Lgals-3 Locus and Different Shape-Types of Heart Remodeling After the First Myocardial Infarction: Preliminary Results. Atherosclerosis. 2017;263:E180-E180
Đorđević Ana D., Živković Maja, Dekleva Milica, Marković-Nikolić Nataša, Alavantić Dragan, Stanković Aleksandra, Đurić Tamara, "Snps in the Vicinity of Lgals-3 Locus and Different Shape-Types of Heart Remodeling After the First Myocardial Infarction: Preliminary Results" Atherosclerosis, 263 (2017):E180-E180,
https://doi.org/10.1016/j.atherosclerosis.2017.06.578 .

RS10757278 FROM 9P21 IS ASSOCIATED WITH ST-ELEVATED MYOCARDIAL INFARCTION IN FEMALES IN POPULATION OF SERBIA

Životić, Ivan; Živković, Maja; Đurić, Tamara; Stanković, Aleksandra; Đorđević, Ana D.; Dekleva, Milica; Marković-Nikolić, Nevena; Alavantić, Dragan

(2017)

TY  - CONF
AU  - Životić, Ivan
AU  - Živković, Maja
AU  - Đurić, Tamara
AU  - Stanković, Aleksandra
AU  - Đorđević, Ana D.
AU  - Dekleva, Milica
AU  - Marković-Nikolić, Nevena
AU  - Alavantić, Dragan
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7178
C3  - Atherosclerosis
T1  - RS10757278 FROM 9P21 IS ASSOCIATED WITH ST-ELEVATED MYOCARDIAL INFARCTION IN FEMALES IN POPULATION OF SERBIA
VL  - 263
SP  - E188
EP  - E188
DO  - 10.1016/j.atherosclerosis.2017.06.603
ER  - 
@conference{
author = "Životić, Ivan and Živković, Maja and Đurić, Tamara and Stanković, Aleksandra and Đorđević, Ana D. and Dekleva, Milica and Marković-Nikolić, Nevena and Alavantić, Dragan",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/7178",
journal = "Atherosclerosis",
title = "RS10757278 FROM 9P21 IS ASSOCIATED WITH ST-ELEVATED MYOCARDIAL INFARCTION IN FEMALES IN POPULATION OF SERBIA",
volume = "263",
pages = "E188-E188",
doi = "10.1016/j.atherosclerosis.2017.06.603"
}
Životić, I., Živković, M., Đurić, T., Stanković, A., Đorđević, A. D., Dekleva, M., Marković-Nikolić, N.,& Alavantić, D. (2017). RS10757278 FROM 9P21 IS ASSOCIATED WITH ST-ELEVATED MYOCARDIAL INFARCTION IN FEMALES IN POPULATION OF SERBIA.
Atherosclerosis, 263, E188-E188.
https://doi.org/10.1016/j.atherosclerosis.2017.06.603
Životić I, Živković M, Đurić T, Stanković A, Đorđević AD, Dekleva M, Marković-Nikolić N, Alavantić D. RS10757278 FROM 9P21 IS ASSOCIATED WITH ST-ELEVATED MYOCARDIAL INFARCTION IN FEMALES IN POPULATION OF SERBIA. Atherosclerosis. 2017;263:E188-E188
Životić Ivan, Živković Maja, Đurić Tamara, Stanković Aleksandra, Đorđević Ana D., Dekleva Milica, Marković-Nikolić Nevena, Alavantić Dragan, "RS10757278 FROM 9P21 IS ASSOCIATED WITH ST-ELEVATED MYOCARDIAL INFARCTION IN FEMALES IN POPULATION OF SERBIA" Atherosclerosis, 263 (2017):E188-E188,
https://doi.org/10.1016/j.atherosclerosis.2017.06.603 .

Heart failure development and rs2274273 in the vicinity of LGALS-3 locus, LGALS-3 relative mRNA expression in patients with first myocardial infarction

Dekleva, Milica; Đorđević, Ana D.; Živković, Maja; Stanković, Aleksandra; Nikolic, N. M. Markovic; Đurić, Tamara

(2017)

TY  - CONF
AU  - Dekleva, Milica
AU  - Đorđević, Ana D.
AU  - Živković, Maja
AU  - Stanković, Aleksandra
AU  - Nikolic, N. M. Markovic
AU  - Đurić, Tamara
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1564
C3  - European Journal of Heart Failure
T1  - Heart failure development and rs2274273 in the vicinity of LGALS-3 locus, LGALS-3 relative mRNA expression in patients with first myocardial infarction
VL  - 19
IS  - SI
SP  - 552
EP  - 552
ER  - 
@conference{
author = "Dekleva, Milica and Đorđević, Ana D. and Živković, Maja and Stanković, Aleksandra and Nikolic, N. M. Markovic and Đurić, Tamara",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1564",
journal = "European Journal of Heart Failure",
title = "Heart failure development and rs2274273 in the vicinity of LGALS-3 locus, LGALS-3 relative mRNA expression in patients with first myocardial infarction",
volume = "19",
number = "SI",
pages = "552-552"
}
Dekleva, M., Đorđević, A. D., Živković, M., Stanković, A., Nikolic, N. M. M.,& Đurić, T. (2017). Heart failure development and rs2274273 in the vicinity of LGALS-3 locus, LGALS-3 relative mRNA expression in patients with first myocardial infarction.
European Journal of Heart Failure, 19(SI), 552-552.
Dekleva M, Đorđević AD, Živković M, Stanković A, Nikolic NMM, Đurić T. Heart failure development and rs2274273 in the vicinity of LGALS-3 locus, LGALS-3 relative mRNA expression in patients with first myocardial infarction. European Journal of Heart Failure. 2017;19(SI):552-552
Dekleva Milica, Đorđević Ana D., Živković Maja, Stanković Aleksandra, Nikolic N. M. Markovic, Đurić Tamara, "Heart failure development and rs2274273 in the vicinity of LGALS-3 locus, LGALS-3 relative mRNA expression in patients with first myocardial infarction" European Journal of Heart Failure, 19, no. SI (2017):552-552

Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression

Prodanović, Radiša; Korićanac, Goran; Vujanac, Ivan; Đorđević, Ana D.; Pantelić, Marija; Romić, Snježana Đ.; Stanimirovic, Zoran; Kirovski, Danijela

(2016)

TY  - JOUR
AU  - Prodanović, Radiša
AU  - Korićanac, Goran
AU  - Vujanac, Ivan
AU  - Đorđević, Ana D.
AU  - Pantelić, Marija
AU  - Romić, Snježana Đ.
AU  - Stanimirovic, Zoran
AU  - Kirovski, Danijela
PY  - 2016
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1211
AB  - We investigated the hypothesis that obesity in dairy cows enhanced expression of proteins involved in hepatic fatty acid uptake and metabolism. Sixteen Holstein-Friesian close-up cows were divided into 2 equal groups based on their body condition score (BCS) as optimal (3.25 LT = BCS LT = 3.5) and high (4.0 LT = BCS LT = 425). Intravenous glucose tolerance test (GTT) and liver biopsies were carried out at day 10 before calving. Blood samples were collected before (basal) and after glucose infusion, and glucose, insulin and non-esterified fatty acid (NEFA) levels were determined at each sample point. In addition, beta-hydroxybutyrate and triglycerides levels were measured in the basal samples. The liver biopsies were analyzed for total lipid content and protein expression of insulin receptor beta (IR beta), fatty acid translocase (FAT/CD36) and sterol regulatory element-binding protein-1 (SREBP-1). Basal glucose and insulin were higher in high-BCS cows, which coincided with higher circulating triglycerides and hepatic lipid content. Clearance rate and AUC for NEFA during GTT were higher in optimal-BCS cows. The development of insulin resistance and fatty liver in obese cows was paralleled by increased hepatic expression of the IR beta, CD36 and SREBP-1. These results suggest that increased expression of hepatic CD36 and SREBP-1 is relevant in the obesity-driven lipid accumulation in the liver of dairy cows during late gestation. (C) 2016 Elsevier Ltd. All rights reserved.
T2  - Research in Veterinary Science
T1  - Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression
VL  - 107
SP  - 16
EP  - 19
DO  - 10.1016/j.rvsc.2016.04.007
ER  - 
@article{
author = "Prodanović, Radiša and Korićanac, Goran and Vujanac, Ivan and Đorđević, Ana D. and Pantelić, Marija and Romić, Snježana Đ. and Stanimirovic, Zoran and Kirovski, Danijela",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1211",
abstract = "We investigated the hypothesis that obesity in dairy cows enhanced expression of proteins involved in hepatic fatty acid uptake and metabolism. Sixteen Holstein-Friesian close-up cows were divided into 2 equal groups based on their body condition score (BCS) as optimal (3.25 LT = BCS LT = 3.5) and high (4.0 LT = BCS LT = 425). Intravenous glucose tolerance test (GTT) and liver biopsies were carried out at day 10 before calving. Blood samples were collected before (basal) and after glucose infusion, and glucose, insulin and non-esterified fatty acid (NEFA) levels were determined at each sample point. In addition, beta-hydroxybutyrate and triglycerides levels were measured in the basal samples. The liver biopsies were analyzed for total lipid content and protein expression of insulin receptor beta (IR beta), fatty acid translocase (FAT/CD36) and sterol regulatory element-binding protein-1 (SREBP-1). Basal glucose and insulin were higher in high-BCS cows, which coincided with higher circulating triglycerides and hepatic lipid content. Clearance rate and AUC for NEFA during GTT were higher in optimal-BCS cows. The development of insulin resistance and fatty liver in obese cows was paralleled by increased hepatic expression of the IR beta, CD36 and SREBP-1. These results suggest that increased expression of hepatic CD36 and SREBP-1 is relevant in the obesity-driven lipid accumulation in the liver of dairy cows during late gestation. (C) 2016 Elsevier Ltd. All rights reserved.",
journal = "Research in Veterinary Science",
title = "Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression",
volume = "107",
pages = "16-19",
doi = "10.1016/j.rvsc.2016.04.007"
}
Prodanović, R., Korićanac, G., Vujanac, I., Đorđević, A. D., Pantelić, M., Romić, S. Đ., Stanimirovic, Z.,& Kirovski, D. (2016). Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression.
Research in Veterinary Science, 107, 16-19.
https://doi.org/10.1016/j.rvsc.2016.04.007
Prodanović R, Korićanac G, Vujanac I, Đorđević AD, Pantelić M, Romić SĐ, Stanimirovic Z, Kirovski D. Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression. Research in Veterinary Science. 2016;107:16-19
Prodanović Radiša, Korićanac Goran, Vujanac Ivan, Đorđević Ana D., Pantelić Marija, Romić Snježana Đ., Stanimirovic Zoran, Kirovski Danijela, "Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression" Research in Veterinary Science, 107 (2016):16-19,
https://doi.org/10.1016/j.rvsc.2016.04.007 .
15
12
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Rs2274273 from LGALS-3 locus and cardiac ventricular remodeling after first myocardial infarction: preliminary results

Đorđević, Ana D.; Đurić, Tamara; Živković, Maja; Životić, Ivan; Dekleva, Milica; Marković-Nikolić, Nataša; Alavantić, Dragan; Stanković, Aleksandra

(2016)

TY  - CONF
AU  - Đorđević, Ana D.
AU  - Đurić, Tamara
AU  - Živković, Maja
AU  - Životić, Ivan
AU  - Dekleva, Milica
AU  - Marković-Nikolić, Nataša
AU  - Alavantić, Dragan
AU  - Stanković, Aleksandra
PY  - 2016
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1101
C3  - European Journal of Heart Failure
T1  - Rs2274273 from LGALS-3 locus and cardiac ventricular remodeling after first myocardial infarction: preliminary results
VL  - 18
IS  - SI
SP  - 283
EP  - 284
ER  - 
@conference{
author = "Đorđević, Ana D. and Đurić, Tamara and Živković, Maja and Životić, Ivan and Dekleva, Milica and Marković-Nikolić, Nataša and Alavantić, Dragan and Stanković, Aleksandra",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1101",
journal = "European Journal of Heart Failure",
title = "Rs2274273 from LGALS-3 locus and cardiac ventricular remodeling after first myocardial infarction: preliminary results",
volume = "18",
number = "SI",
pages = "283-284"
}
Đorđević, A. D., Đurić, T., Živković, M., Životić, I., Dekleva, M., Marković-Nikolić, N., Alavantić, D.,& Stanković, A. (2016). Rs2274273 from LGALS-3 locus and cardiac ventricular remodeling after first myocardial infarction: preliminary results.
European Journal of Heart Failure, 18(SI), 283-284.
Đorđević AD, Đurić T, Živković M, Životić I, Dekleva M, Marković-Nikolić N, Alavantić D, Stanković A. Rs2274273 from LGALS-3 locus and cardiac ventricular remodeling after first myocardial infarction: preliminary results. European Journal of Heart Failure. 2016;18(SI):283-284
Đorđević Ana D., Đurić Tamara, Živković Maja, Životić Ivan, Dekleva Milica, Marković-Nikolić Nataša, Alavantić Dragan, Stanković Aleksandra, "Rs2274273 from LGALS-3 locus and cardiac ventricular remodeling after first myocardial infarction: preliminary results" European Journal of Heart Failure, 18, no. SI (2016):283-284

Genetic Variants in the Vicinity of LGALS-3 Gene and LGALS-3 mRNA Expression in Advanced Carotid Atherosclerosis: An Exploratory Study

Đorđević, Ana D.; Živković, Maja; Stanković, Aleksandra; Životić, Ivan; Končar, Igor; Davidovic, Lazar; Alavantić, Dragan; Đurić, Tamara

(2016)

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Živković, Maja
AU  - Stanković, Aleksandra
AU  - Životić, Ivan
AU  - Končar, Igor
AU  - Davidovic, Lazar
AU  - Alavantić, Dragan
AU  - Đurić, Tamara
PY  - 2016
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1291
AB  - BackgroundPrevious research has shown that there is an association between galectin-3 (gal-3) protein and cardiovascular pathology. The aim of this study was to investigate the effects of rs2274273 and rs17128183 on genetic susceptibility to advanced carotid atherosclerosis (CA) and its complications. The rs2274273 has been singled out as the lead SNP of the haplotype block containing LGALS-3 (gal-3 gene) associated with gal-3 circulating levels, while rs17128183 constitutes a potentially functional SNP of the same hap-block. We further sought to determine whether these genetic variants have an impact on the expression of LGALS-3 mRNA in human carotid atherosclerotic plaque tissue. MethodsThe study encompassed 300 control subjects and 485 patients with advanced CA who had undergone carotid endarterectomy. Rs2274273, rs17128183, and LGALS-3 relative mRNA expression was detected by means of real-time PCR (TaqMan((R)) technology). ResultsThere were no statistically significant associations of the investigated genetic variants with susceptibility to advanced CA, nor did we find any associations in terms of ultrasonographically defined plaque phenotypes. The relative expression of LGALS-3 mRNA proved to be significantly higher in carriers of the rare alleles (P=0.039) for both genetic variants. ConclusionOur exploratory results suggest that while rs2274273 and rs17128183 bear no association with the risk of advanced CA or CA-related complications, these genetic variants are likely to affect LGALS-3 expression levels. In order to reach a definitive conclusion on the role played by rs2274273 and rs17128183 in advanced CA, our results should be further validated.
T2  - Journal of Clinical Laboratory Analysis
T1  - Genetic Variants in the Vicinity of LGALS-3 Gene and LGALS-3 mRNA Expression in Advanced Carotid Atherosclerosis: An Exploratory Study
VL  - 30
IS  - 6
SP  - 1150
EP  - 1157
DO  - 10.1002/jcla.21996
ER  - 
@article{
author = "Đorđević, Ana D. and Živković, Maja and Stanković, Aleksandra and Životić, Ivan and Končar, Igor and Davidovic, Lazar and Alavantić, Dragan and Đurić, Tamara",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1291",
abstract = "BackgroundPrevious research has shown that there is an association between galectin-3 (gal-3) protein and cardiovascular pathology. The aim of this study was to investigate the effects of rs2274273 and rs17128183 on genetic susceptibility to advanced carotid atherosclerosis (CA) and its complications. The rs2274273 has been singled out as the lead SNP of the haplotype block containing LGALS-3 (gal-3 gene) associated with gal-3 circulating levels, while rs17128183 constitutes a potentially functional SNP of the same hap-block. We further sought to determine whether these genetic variants have an impact on the expression of LGALS-3 mRNA in human carotid atherosclerotic plaque tissue. MethodsThe study encompassed 300 control subjects and 485 patients with advanced CA who had undergone carotid endarterectomy. Rs2274273, rs17128183, and LGALS-3 relative mRNA expression was detected by means of real-time PCR (TaqMan((R)) technology). ResultsThere were no statistically significant associations of the investigated genetic variants with susceptibility to advanced CA, nor did we find any associations in terms of ultrasonographically defined plaque phenotypes. The relative expression of LGALS-3 mRNA proved to be significantly higher in carriers of the rare alleles (P=0.039) for both genetic variants. ConclusionOur exploratory results suggest that while rs2274273 and rs17128183 bear no association with the risk of advanced CA or CA-related complications, these genetic variants are likely to affect LGALS-3 expression levels. In order to reach a definitive conclusion on the role played by rs2274273 and rs17128183 in advanced CA, our results should be further validated.",
journal = "Journal of Clinical Laboratory Analysis",
title = "Genetic Variants in the Vicinity of LGALS-3 Gene and LGALS-3 mRNA Expression in Advanced Carotid Atherosclerosis: An Exploratory Study",
volume = "30",
number = "6",
pages = "1150-1157",
doi = "10.1002/jcla.21996"
}
Đorđević, A. D., Živković, M., Stanković, A., Životić, I., Končar, I., Davidovic, L., Alavantić, D.,& Đurić, T. (2016). Genetic Variants in the Vicinity of LGALS-3 Gene and LGALS-3 mRNA Expression in Advanced Carotid Atherosclerosis: An Exploratory Study.
Journal of Clinical Laboratory Analysis, 30(6), 1150-1157.
https://doi.org/10.1002/jcla.21996
Đorđević AD, Živković M, Stanković A, Životić I, Končar I, Davidovic L, Alavantić D, Đurić T. Genetic Variants in the Vicinity of LGALS-3 Gene and LGALS-3 mRNA Expression in Advanced Carotid Atherosclerosis: An Exploratory Study. Journal of Clinical Laboratory Analysis. 2016;30(6):1150-1157
Đorđević Ana D., Živković Maja, Stanković Aleksandra, Životić Ivan, Končar Igor, Davidovic Lazar, Alavantić Dragan, Đurić Tamara, "Genetic Variants in the Vicinity of LGALS-3 Gene and LGALS-3 mRNA Expression in Advanced Carotid Atherosclerosis: An Exploratory Study" Journal of Clinical Laboratory Analysis, 30, no. 6 (2016):1150-1157,
https://doi.org/10.1002/jcla.21996 .
6
5
5

9p21 locus rs10757278 is associated with advanced carotid atherosclerosis in a gender-specific manner

Životić, Ivan; Đurić, Tamara; Stanković, Aleksandra; Đorđević, Ana D.; Končar, Igor; Davidovic, Lazar; Alavantić, Dragan; Živković, Maja

(2016)

TY  - JOUR
AU  - Životić, Ivan
AU  - Đurić, Tamara
AU  - Stanković, Aleksandra
AU  - Đorđević, Ana D.
AU  - Končar, Igor
AU  - Davidovic, Lazar
AU  - Alavantić, Dragan
AU  - Živković, Maja
PY  - 2016
UR  - http://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 D. and Končar, Igor and Davidovic, Lazar and Alavantić, Dragan and Živković, Maja",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1126",
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. D., Končar, I., Davidovic, L., Alavantić, D.,& Živković, M. (2016). 9p21 locus rs10757278 is associated with advanced carotid atherosclerosis in a gender-specific manner.
Experimental Biology and Medicine, 241(11), 1210-1216.
https://doi.org/10.1177/1535370216636718
Životić I, Đurić T, Stanković A, Đorđević AD, Končar I, Davidovic L, Alavantić D, Živković M. 9p21 locus rs10757278 is associated with advanced carotid atherosclerosis in a gender-specific manner. Experimental Biology and Medicine. 2016;241(11):1210-1216
Životić Ivan, Đurić Tamara, Stanković Aleksandra, Đorđević Ana D., Končar Igor, Davidovic Lazar, Alavantić Dragan, Živković Maja, "9p21 locus rs10757278 is associated with advanced carotid atherosclerosis in a gender-specific manner" Experimental Biology and Medicine, 241, no. 11 (2016):1210-1216,
https://doi.org/10.1177/1535370216636718 .
1
3
3
4

Alterations in the Nrf2-Keap1 signaling pathway and its downstream target genes in rat brain under stress

Đorđević, Jelena D.; Đorđević, Ana D.; Adžić, Miroslav; Mitić, Miloš; Lukić, Iva; Radoičić, Marija B.

(2015)

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Mitić, Miloš
AU  - Lukić, Iva
AU  - Radoičić, Marija B.
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/270
AB  - Knowledge of the antioxidant defense in the stress-responding structures of the CNS is of crucial importance, since oxidative damage is a phenomenon accompanying many stress-related disorders. Regulation of antioxidative and anti-inflammatory defense through Nrf2 (nuclear factor 2 eritroid related factor 2) pathway has emerged as a promising approach for neuroprotection. In this study, we used chronic social isolation of male Wistar rats to induce depressive-like behavior. We hypothesized that Nrf2 Keap1 pathway is compromised in the limbic brain after prolonged stress. Since subcellular trafficking of Nrf2 and its inhibitor Keap1 (Kelch ECH associating protein 1) is essential for the activation of Nrf2, we determined their protein level in cytosolic and nuclear comp and linents of hippocampus and prefrontal cortex (PEG). We also determined mRNA levels of Nr12-regulated genes involved in the production and utilization of glutathione, glutamate cysteine ligase (Gclm), glutathione S-transferase (Gsta3) and glutathione reductase (Gsr). Our results showed that chronic isolation induced anxiety and depressive-like behavior, decreased Nrf2 and in parallel increased Keap1 and nuclear factor kappa B (NF kappa B) in the hippocampus, which were not accompanied by expression profiles of Nrf2-regulated genes. Chronically stressed rats challenged with acute stress failed to induce any response of examined genes in either of brain structures, even though Nrf2/Keap1 was altered, while in naive animals Nrf2 activity corresponded witli an expression of Nrf2-regulated genes. Our results reveal maladaptive character of chronic stress at Nrf2/Keap1 level followed by pro-inflammatory conditions, and suggest a possible role of these alterations in pathogenesis of depressive/anxiety disorders. (C) 2015 Elsevier B.V. All rights reserved.
T2  - Brain Research
T1  - Alterations in the Nrf2-Keap1 signaling pathway and its downstream target genes in rat brain under stress
VL  - 1602
SP  - 20
EP  - 31
DO  - 10.1016/j.brainres.2015.01.010
ER  - 
@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Mitić, Miloš and Lukić, Iva and Radoičić, Marija B.",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/270",
abstract = "Knowledge of the antioxidant defense in the stress-responding structures of the CNS is of crucial importance, since oxidative damage is a phenomenon accompanying many stress-related disorders. Regulation of antioxidative and anti-inflammatory defense through Nrf2 (nuclear factor 2 eritroid related factor 2) pathway has emerged as a promising approach for neuroprotection. In this study, we used chronic social isolation of male Wistar rats to induce depressive-like behavior. We hypothesized that Nrf2 Keap1 pathway is compromised in the limbic brain after prolonged stress. Since subcellular trafficking of Nrf2 and its inhibitor Keap1 (Kelch ECH associating protein 1) is essential for the activation of Nrf2, we determined their protein level in cytosolic and nuclear comp and linents of hippocampus and prefrontal cortex (PEG). We also determined mRNA levels of Nr12-regulated genes involved in the production and utilization of glutathione, glutamate cysteine ligase (Gclm), glutathione S-transferase (Gsta3) and glutathione reductase (Gsr). Our results showed that chronic isolation induced anxiety and depressive-like behavior, decreased Nrf2 and in parallel increased Keap1 and nuclear factor kappa B (NF kappa B) in the hippocampus, which were not accompanied by expression profiles of Nrf2-regulated genes. Chronically stressed rats challenged with acute stress failed to induce any response of examined genes in either of brain structures, even though Nrf2/Keap1 was altered, while in naive animals Nrf2 activity corresponded witli an expression of Nrf2-regulated genes. Our results reveal maladaptive character of chronic stress at Nrf2/Keap1 level followed by pro-inflammatory conditions, and suggest a possible role of these alterations in pathogenesis of depressive/anxiety disorders. (C) 2015 Elsevier B.V. All rights reserved.",
journal = "Brain Research",
title = "Alterations in the Nrf2-Keap1 signaling pathway and its downstream target genes in rat brain under stress",
volume = "1602",
pages = "20-31",
doi = "10.1016/j.brainres.2015.01.010"
}
Đorđević, J. D., Đorđević, A. D., Adžić, M., Mitić, M., Lukić, I.,& Radoičić, M. B. (2015). Alterations in the Nrf2-Keap1 signaling pathway and its downstream target genes in rat brain under stress.
Brain Research, 1602, 20-31.
https://doi.org/10.1016/j.brainres.2015.01.010
Đorđević JD, Đorđević AD, Adžić M, Mitić M, Lukić I, Radoičić MB. Alterations in the Nrf2-Keap1 signaling pathway and its downstream target genes in rat brain under stress. Brain Research. 2015;1602:20-31
Đorđević Jelena D., Đorđević Ana D., Adžić Miroslav, Mitić Miloš, Lukić Iva, Radoičić Marija B., "Alterations in the Nrf2-Keap1 signaling pathway and its downstream target genes in rat brain under stress" Brain Research, 1602 (2015):20-31,
https://doi.org/10.1016/j.brainres.2015.01.010 .
43
38
46

Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver

Dobutovic, Branislava; Sudar, Emina; Tepavčević, Snežana; Đorđević, Jelena D.; Đorđević, Ana D.; Radoičić, Marija B.; Isenović, Esma R.

(2014)

TY  - JOUR
AU  - Dobutovic, Branislava
AU  - Sudar, Emina
AU  - Tepavčević, Snežana
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Radoičić, Marija B.
AU  - Isenović, Esma R.
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/93
AB  - Introduction: We investigated the effects of ghrelin on protein expression of the liver antioxidant enzymes superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), nuclear factor kappa B (NF kappa B) and inducible nitric oxide synthase (iNOS). Furthermore, we aimed to investigate whether extracellular regulated protein kinase (ERK1/2) and protein kinase B (Akt) are involved in ghrelin-regulated liver antioxidant enzymes and iNOS protein expression. Material and methods: Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) injected into the lateral cerebral ventricle every 24 h for 5 days, and 2 h after the last treatment the animals were sacrificed and the liver excised. The Western blot method was used to determine expression of antioxidant enzymes, iNOS, phosphorylation of Akt, ERK1/2 and nuclear factor kappa B (NF kappa B) subunits 50 and 65. Results: There was significantly higher protein expression of CuZnSOD (p LT 0.001), MnSOD (p LT 0.001), CAT (p LT 0.001), GPx, (p LT 0.001), and GR (p LT 0.01) in the liver isolated from ghrelin-treated animals compared with control animals. In contrast, ghrelin significantly (p LT 0.01) reduced protein expression of iNOS. In addition, phosphorylation of NF kappa B subunits p65 and p50 was significantly (p LT 0.001 for p65; p LT 0.05 for p50) reduced by ghrelin when compared with controls. Phosphorylation of ERK1/2 and of Akt was significantly higher in ghrelin-treated than in control animals (p LT 0.05 for ERK1/2; p LT 0.01 for Akt). Conclusions: The results show that activation of Akt and ERK1/2 is involved in ghrelin-mediated regulation of protein expression of antioxidant enzymes and iNOS in the rat liver.
T2  - Archives of Medical Science
T1  - Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver
VL  - 10
IS  - 4
SP  - 806
EP  - 816
DO  - 10.5114/aoms.2014.44872
ER  - 
@article{
author = "Dobutovic, Branislava and Sudar, Emina and Tepavčević, Snežana and Đorđević, Jelena D. and Đorđević, Ana D. and Radoičić, Marija B. and Isenović, Esma R.",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/93",
abstract = "Introduction: We investigated the effects of ghrelin on protein expression of the liver antioxidant enzymes superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), nuclear factor kappa B (NF kappa B) and inducible nitric oxide synthase (iNOS). Furthermore, we aimed to investigate whether extracellular regulated protein kinase (ERK1/2) and protein kinase B (Akt) are involved in ghrelin-regulated liver antioxidant enzymes and iNOS protein expression. Material and methods: Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) injected into the lateral cerebral ventricle every 24 h for 5 days, and 2 h after the last treatment the animals were sacrificed and the liver excised. The Western blot method was used to determine expression of antioxidant enzymes, iNOS, phosphorylation of Akt, ERK1/2 and nuclear factor kappa B (NF kappa B) subunits 50 and 65. Results: There was significantly higher protein expression of CuZnSOD (p LT 0.001), MnSOD (p LT 0.001), CAT (p LT 0.001), GPx, (p LT 0.001), and GR (p LT 0.01) in the liver isolated from ghrelin-treated animals compared with control animals. In contrast, ghrelin significantly (p LT 0.01) reduced protein expression of iNOS. In addition, phosphorylation of NF kappa B subunits p65 and p50 was significantly (p LT 0.001 for p65; p LT 0.05 for p50) reduced by ghrelin when compared with controls. Phosphorylation of ERK1/2 and of Akt was significantly higher in ghrelin-treated than in control animals (p LT 0.05 for ERK1/2; p LT 0.01 for Akt). Conclusions: The results show that activation of Akt and ERK1/2 is involved in ghrelin-mediated regulation of protein expression of antioxidant enzymes and iNOS in the rat liver.",
journal = "Archives of Medical Science",
title = "Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver",
volume = "10",
number = "4",
pages = "806-816",
doi = "10.5114/aoms.2014.44872"
}
Dobutovic, B., Sudar, E., Tepavčević, S., Đorđević, J. D., Đorđević, A. D., Radoičić, M. B.,& Isenović, E. R. (2014). Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver.
Archives of Medical Science, 10(4), 806-816.
https://doi.org/10.5114/aoms.2014.44872
Dobutovic B, Sudar E, Tepavčević S, Đorđević JD, Đorđević AD, Radoičić MB, Isenović ER. Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver. Archives of Medical Science. 2014;10(4):806-816
Dobutovic Branislava, Sudar Emina, Tepavčević Snežana, Đorđević Jelena D., Đorđević Ana D., Radoičić Marija B., Isenović Esma R., "Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver" Archives of Medical Science, 10, no. 4 (2014):806-816,
https://doi.org/10.5114/aoms.2014.44872 .
18
17
22

Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism

Adžić, Miroslav; Lukić, Iva; Mitić, Miloš; Đorđević, Jelena D.; Elakovic, Ivana; Đorđević, Ana D.; Krstic-Demonacos, Marija; Matić, Gordana; Radoičić, Marija B.

(2013)

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Lukić, Iva
AU  - Mitić, Miloš
AU  - Đorđević, Jelena D.
AU  - Elakovic, Ivana
AU  - Đorđević, Ana D.
AU  - Krstic-Demonacos, Marija
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5868
AB  - Antidepressants affect glucocorticoid receptor (GR) functioning partly through modulation of its phosphorylation but their effects on mitochondrial GR have remained undefined. We investigated the ability of chronic fiuoxetine treatment to affect chronic stress-induced changes of mitochondrial GR and its phosphoisoforms (pGRs) in the prefrontal cortex and hippocampus of female and male rats. Since mitochondrial GR regulates oxidative phosphorylation, expression of mitochondrial-encoded subunits of cytochrome (cyt) c oxidase and its activity were also investigated. Chronic stress caused accumulation of the GR in mitochondria of female prefrontal cortex, while the changes in the hippocampus were sex-specific at the levels of pGRs. Expression of mitochondrial COXs genes corresponded to chronic stress-modulated mitochondrial GR in both tissues of both genders and to cyt c oxidase activity in females. Moreover, the metabolic parameters in stressed animals were affected by fiuoxetine therapy only in the hippocampus. Namely, fluoxetine effects on mitochondrial COXs and cyt c oxidase activity in the hippocampus seem to be conveyed through pGR232 in females, while in males this likely occurs through other mechanisms. In summary, sex-specific regulation of cyt c oxidase by the stress and antidepressant treatment and its differential convergence with mitochondrial GR signaling in the prefrontal cortex and hippocampus could contribute to clarification of sex-dependent vulnerability to stress-related disorders and sex-specific clinical impact of antidepressants. (C) 2013 Elsevier Ltd. All rights reserved.
T2  - Psychoneuroendocrinology
T1  - Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism
VL  - 38
IS  - 12
SP  - 2914
EP  - 2924
DO  - 10.1016/j.psyneuen.2013.07.019
ER  - 
@article{
author = "Adžić, Miroslav and Lukić, Iva and Mitić, Miloš and Đorđević, Jelena D. and Elakovic, Ivana and Đorđević, Ana D. and Krstic-Demonacos, Marija and Matić, Gordana and Radoičić, Marija B.",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5868",
abstract = "Antidepressants affect glucocorticoid receptor (GR) functioning partly through modulation of its phosphorylation but their effects on mitochondrial GR have remained undefined. We investigated the ability of chronic fiuoxetine treatment to affect chronic stress-induced changes of mitochondrial GR and its phosphoisoforms (pGRs) in the prefrontal cortex and hippocampus of female and male rats. Since mitochondrial GR regulates oxidative phosphorylation, expression of mitochondrial-encoded subunits of cytochrome (cyt) c oxidase and its activity were also investigated. Chronic stress caused accumulation of the GR in mitochondria of female prefrontal cortex, while the changes in the hippocampus were sex-specific at the levels of pGRs. Expression of mitochondrial COXs genes corresponded to chronic stress-modulated mitochondrial GR in both tissues of both genders and to cyt c oxidase activity in females. Moreover, the metabolic parameters in stressed animals were affected by fiuoxetine therapy only in the hippocampus. Namely, fluoxetine effects on mitochondrial COXs and cyt c oxidase activity in the hippocampus seem to be conveyed through pGR232 in females, while in males this likely occurs through other mechanisms. In summary, sex-specific regulation of cyt c oxidase by the stress and antidepressant treatment and its differential convergence with mitochondrial GR signaling in the prefrontal cortex and hippocampus could contribute to clarification of sex-dependent vulnerability to stress-related disorders and sex-specific clinical impact of antidepressants. (C) 2013 Elsevier Ltd. All rights reserved.",
journal = "Psychoneuroendocrinology",
title = "Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism",
volume = "38",
number = "12",
pages = "2914-2924",
doi = "10.1016/j.psyneuen.2013.07.019"
}
Adžić, M., Lukić, I., Mitić, M., Đorđević, J. D., Elakovic, I., Đorđević, A. D., Krstic-Demonacos, M., Matić, G.,& Radoičić, M. B. (2013). Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism.
Psychoneuroendocrinology, 38(12), 2914-2924.
https://doi.org/10.1016/j.psyneuen.2013.07.019
Adžić M, Lukić I, Mitić M, Đorđević JD, Elakovic I, Đorđević AD, Krstic-Demonacos M, Matić G, Radoičić MB. Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism. Psychoneuroendocrinology. 2013;38(12):2914-2924
Adžić Miroslav, Lukić Iva, Mitić Miloš, Đorđević Jelena D., Elakovic Ivana, Đorđević Ana D., Krstic-Demonacos Marija, Matić Gordana, Radoičić Marija B., "Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism" Psychoneuroendocrinology, 38, no. 12 (2013):2914-2924,
https://doi.org/10.1016/j.psyneuen.2013.07.019 .
28
26
26

Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats

Korićanac, Goran; Đorđević, Ana D.; Žakula, Zorica; Vojnovic-Milutinovic, Danijela; Tepavčević, Snežana; Velikovic, Natasa; Milosavljević, Tijana; Stojiljković, Mojca D.; Romić, Snježana Đ.; Matić, Gordana

(2013)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Đorđević, Ana D.
AU  - Žakula, Zorica
AU  - Vojnovic-Milutinovic, Danijela
AU  - Tepavčević, Snežana
AU  - Velikovic, Natasa
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Romić, Snježana Đ.
AU  - Matić, Gordana
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5507
AB  - We analyzed the effects of a fructose-rich diet (FRD) to test the assumption that the expression of metabolic syndrome phenotype is different in male and female rats. Two-way ANOVA revealed a significant effect of FRD on feeding behavior and carbohydrate/lipid metabolism. The increased caloric intake in FRD rats of both sexes was followed by a cluster of gender-specific changes typical for the metabolic syndrome. Female rats were characterized by decreased glycemia, increased triglycerides, enlarged visceral adipose tissue and increased absolute mass of liver, without changes in systolic blood pressure and insulin sensitivity. In contrast, male rats developed less disturbances in physical and biochemical characteristics, but blood pressure and insulin sensitivity were impaired by FRD. The results emphasize the detrimental effects of fructose consumption on cardiovascular risk and insulin action in males, whereas females are affected by other metabolic disturbances. These results support the idea of gender-dependent differences in the expression of the metabolic syndrome phenotype.
T2  - Archives of biological sciences
T1  - Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats
VL  - 65
IS  - 2
SP  - 455
EP  - 464
DO  - 10.2298/ABS1302455K
ER  - 
@article{
author = "Korićanac, Goran and Đorđević, Ana D. and Žakula, Zorica and Vojnovic-Milutinovic, Danijela and Tepavčević, Snežana and Velikovic, Natasa and Milosavljević, Tijana and Stojiljković, Mojca D. and Romić, Snježana Đ. and Matić, Gordana",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5507",
abstract = "We analyzed the effects of a fructose-rich diet (FRD) to test the assumption that the expression of metabolic syndrome phenotype is different in male and female rats. Two-way ANOVA revealed a significant effect of FRD on feeding behavior and carbohydrate/lipid metabolism. The increased caloric intake in FRD rats of both sexes was followed by a cluster of gender-specific changes typical for the metabolic syndrome. Female rats were characterized by decreased glycemia, increased triglycerides, enlarged visceral adipose tissue and increased absolute mass of liver, without changes in systolic blood pressure and insulin sensitivity. In contrast, male rats developed less disturbances in physical and biochemical characteristics, but blood pressure and insulin sensitivity were impaired by FRD. The results emphasize the detrimental effects of fructose consumption on cardiovascular risk and insulin action in males, whereas females are affected by other metabolic disturbances. These results support the idea of gender-dependent differences in the expression of the metabolic syndrome phenotype.",
journal = "Archives of biological sciences",
title = "Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats",
volume = "65",
number = "2",
pages = "455-464",
doi = "10.2298/ABS1302455K"
}
Korićanac, G., Đorđević, A. D., Žakula, Z., Vojnovic-Milutinovic, D., Tepavčević, S., Velikovic, N., Milosavljević, T., Stojiljković, M. D., Romić, S. Đ.,& Matić, G. (2013). Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats.
Archives of biological sciences, 65(2), 455-464.
https://doi.org/10.2298/ABS1302455K
Korićanac G, Đorđević AD, Žakula Z, Vojnovic-Milutinovic D, Tepavčević S, Velikovic N, Milosavljević T, Stojiljković MD, Romić SĐ, Matić G. Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats. Archives of biological sciences. 2013;65(2):455-464
Korićanac Goran, Đorđević Ana D., Žakula Zorica, Vojnovic-Milutinovic Danijela, Tepavčević Snežana, Velikovic Natasa, Milosavljević Tijana, Stojiljković Mojca D., Romić Snježana Đ., Matić Gordana, "Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats" Archives of biological sciences, 65, no. 2 (2013):455-464,
https://doi.org/10.2298/ABS1302455K .
12
12
12

Radiation-Mediated Induction of Apoptotic Cell Death in Rat Hippocampus

Velickovic, Natasa A.; Đorđević, Ana D.; Drakulić, Dunja R.; Šećerov, Bojana Lj.; Grković, Ivana; Milošević, Maja; Horvat, Anica

(2013)

TY  - JOUR
AU  - Velickovic, Natasa A.
AU  - Đorđević, Ana D.
AU  - Drakulić, Dunja R.
AU  - Šećerov, Bojana Lj.
AU  - Grković, Ivana
AU  - Milošević, Maja
AU  - Horvat, Anica
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5594
AB  - Ionizing radiation is commonly used in the treatment of brain tumors but it can impair cognitive functions, such as learning and memory. Since cognitive dysfunctions are predominantly result of cell death by apoptosis in hippocampal cells, in this study we analyzed acute effects of cranial gamma-irradiation (10 Gy) on-expression-of proapoptotic molecules (p53, Box) and antiapoptotic molecule Bcl-2, as well as caspase-3 activation and cytochrome c redistribution in the hippocampus of young rats. The selected regimen of irradiation resembles the established animal model for childhood prophylactic cranial radiotherapy. Our results demonstrated that p53 mRNA expression was unchanged after irradiation, while induction of p53 protein was rapid. In parallel, Bax mRNA and protein levels were also increased following irradiation, whereas Bcl-2 expression was not changed during the examined post-irradiation period. These changes were accompanied with early hallmarks of apoptosis, such as increased cytochrome c release and stimulated activation of caspase-3. Overall, this study demonstrates that cranial irradiation is associated with the augmented apoptotic pathway in the rat hippocampus, which could be related to the cognitive decline observed in patients after prophylactic cranial radiotherapy, but also opens perspective in finding radioprotectors that can mitigate radiation injury of normal brain tissue.
T2  - Nuclear technology and radiation protection
T1  - Radiation-Mediated Induction of Apoptotic Cell Death in Rat Hippocampus
VL  - 28
IS  - 2
SP  - 212
EP  - 220
DO  - 10.2298/NTRP1302212V
ER  - 
@article{
author = "Velickovic, Natasa A. and Đorđević, Ana D. and Drakulić, Dunja R. and Šećerov, Bojana Lj. and Grković, Ivana and Milošević, Maja and Horvat, Anica",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5594",
abstract = "Ionizing radiation is commonly used in the treatment of brain tumors but it can impair cognitive functions, such as learning and memory. Since cognitive dysfunctions are predominantly result of cell death by apoptosis in hippocampal cells, in this study we analyzed acute effects of cranial gamma-irradiation (10 Gy) on-expression-of proapoptotic molecules (p53, Box) and antiapoptotic molecule Bcl-2, as well as caspase-3 activation and cytochrome c redistribution in the hippocampus of young rats. The selected regimen of irradiation resembles the established animal model for childhood prophylactic cranial radiotherapy. Our results demonstrated that p53 mRNA expression was unchanged after irradiation, while induction of p53 protein was rapid. In parallel, Bax mRNA and protein levels were also increased following irradiation, whereas Bcl-2 expression was not changed during the examined post-irradiation period. These changes were accompanied with early hallmarks of apoptosis, such as increased cytochrome c release and stimulated activation of caspase-3. Overall, this study demonstrates that cranial irradiation is associated with the augmented apoptotic pathway in the rat hippocampus, which could be related to the cognitive decline observed in patients after prophylactic cranial radiotherapy, but also opens perspective in finding radioprotectors that can mitigate radiation injury of normal brain tissue.",
journal = "Nuclear technology and radiation protection",
title = "Radiation-Mediated Induction of Apoptotic Cell Death in Rat Hippocampus",
volume = "28",
number = "2",
pages = "212-220",
doi = "10.2298/NTRP1302212V"
}
Velickovic, N. A., Đorđević, A. D., Drakulić, D. R., Šećerov, B. Lj., Grković, I., Milošević, M.,& Horvat, A. (2013). Radiation-Mediated Induction of Apoptotic Cell Death in Rat Hippocampus.
Nuclear technology and radiation protection, 28(2), 212-220.
https://doi.org/10.2298/NTRP1302212V
Velickovic NA, Đorđević AD, Drakulić DR, Šećerov BL, Grković I, Milošević M, Horvat A. Radiation-Mediated Induction of Apoptotic Cell Death in Rat Hippocampus. Nuclear technology and radiation protection. 2013;28(2):212-220
Velickovic Natasa A., Đorđević Ana D., Drakulić Dunja R., Šećerov Bojana Lj., Grković Ivana, Milošević Maja, Horvat Anica, "Radiation-Mediated Induction of Apoptotic Cell Death in Rat Hippocampus" Nuclear technology and radiation protection, 28, no. 2 (2013):212-220,
https://doi.org/10.2298/NTRP1302212V .

Enos Glu298asp Polymorphism Is Associated with Development of Complicated Plaques in Patients from Serbia with Advanced Carotid Atherosclerosis

Đurić, Tamara; Đorđević, Ana D.; Lukic, N.; Andelevski, Magdalena; Živković, Maja; Stanković, Aleksandra

(2013)

TY  - JOUR
AU  - Đurić, Tamara
AU  - Đorđević, Ana D.
AU  - Lukic, N.
AU  - Andelevski, Magdalena
AU  - Živković, Maja
AU  - Stanković, Aleksandra
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5188
AB  - Nitric oxide inhibits adhesion of thrombocytes, proliferation and migration of smooth muscle cells and restricts oxidation of atherogenic low-density lipoproteins. Therefore, decreased production or activity of NO may play a role in the initiation, progression or complications of atherosclerosis. The aim of this study was to estimate the effect of Glu298Asp eNOS gene polymorphism on the individual risk for development of complicated carotid atherosclerotic plaque in patients from Serbia with advanced carotid atherosclerosis (CA) who had undergone endarterectomy. The study population included 233 patients. eNOS G894T gene polymorphism was identified by PCR and RFLP methods. Multivariate logistic regression analysis showed that Asp298Asp is an independent risk factor for the presence of complicated plaques in CA patients. Patients who were homozygous for the Asp298 allele had an adjusted OR of 4.36 for the development of complicated plaques compared to those that carry the Glu298 allele. Further validation and replication studies are needed.
T2  - Archives of biological sciences
T1  - Enos Glu298asp Polymorphism Is Associated with Development of Complicated Plaques in Patients from Serbia with Advanced Carotid Atherosclerosis
VL  - 65
IS  - 1
SP  - 143
EP  - 149
DO  - 10.2298/ABS1301143D
ER  - 
@article{
author = "Đurić, Tamara and Đorđević, Ana D. and Lukic, N. and Andelevski, Magdalena and Živković, Maja and Stanković, Aleksandra",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5188",
abstract = "Nitric oxide inhibits adhesion of thrombocytes, proliferation and migration of smooth muscle cells and restricts oxidation of atherogenic low-density lipoproteins. Therefore, decreased production or activity of NO may play a role in the initiation, progression or complications of atherosclerosis. The aim of this study was to estimate the effect of Glu298Asp eNOS gene polymorphism on the individual risk for development of complicated carotid atherosclerotic plaque in patients from Serbia with advanced carotid atherosclerosis (CA) who had undergone endarterectomy. The study population included 233 patients. eNOS G894T gene polymorphism was identified by PCR and RFLP methods. Multivariate logistic regression analysis showed that Asp298Asp is an independent risk factor for the presence of complicated plaques in CA patients. Patients who were homozygous for the Asp298 allele had an adjusted OR of 4.36 for the development of complicated plaques compared to those that carry the Glu298 allele. Further validation and replication studies are needed.",
journal = "Archives of biological sciences",
title = "Enos Glu298asp Polymorphism Is Associated with Development of Complicated Plaques in Patients from Serbia with Advanced Carotid Atherosclerosis",
volume = "65",
number = "1",
pages = "143-149",
doi = "10.2298/ABS1301143D"
}
Đurić, T., Đorđević, A. D., Lukic, N., Andelevski, M., Živković, M.,& Stanković, A. (2013). Enos Glu298asp Polymorphism Is Associated with Development of Complicated Plaques in Patients from Serbia with Advanced Carotid Atherosclerosis.
Archives of biological sciences, 65(1), 143-149.
https://doi.org/10.2298/ABS1301143D
Đurić T, Đorđević AD, Lukic N, Andelevski M, Živković M, Stanković A. Enos Glu298asp Polymorphism Is Associated with Development of Complicated Plaques in Patients from Serbia with Advanced Carotid Atherosclerosis. Archives of biological sciences. 2013;65(1):143-149
Đurić Tamara, Đorđević Ana D., Lukic N., Andelevski Magdalena, Živković Maja, Stanković Aleksandra, "Enos Glu298asp Polymorphism Is Associated with Development of Complicated Plaques in Patients from Serbia with Advanced Carotid Atherosclerosis" Archives of biological sciences, 65, no. 1 (2013):143-149,
https://doi.org/10.2298/ABS1301143D .
1

Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats

Đorđević, Ana D.; Đorđević, Jelena D.; Elakovic, Ivana; Adžić, Miroslav; Matić, Gordana; Radoičić, Marija B.

(2012)

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Elakovic, Ivana
AU  - Adžić, Miroslav
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4678
AB  - Plastic response and successful adaptation to stress are of particular importance in the hippocampus, where chronic stress may cause cell death instead of neural remodeling. Structural modifications that occur both in the brain of depressed patients and animal stress models may be reversed by antidepressants. Since morphological changes induced by stress and/or antidepressants could be mediated by presynaptically located proteins, determining the levels of these proteins may be a useful way to identify molecular changes associated with synaptic plasticity. In this study we analyzed the effects of chronic (six-week) social isolation and long-term (three-week) fluoxetine treatment on molecular markers of plasticity and apoptosis in the hippocampus of Wistar rats. Compartmental redistribution of NF kappa B transcription factor involved in the regulation of plasticity and apoptosis was also examined. To establish whether social isolation is able to evoke behavioral-like effects, which might be related to the observed molecular changes, we performed the forced swimming test. The results show that synaptosomal polysialic neural cell adhesion molecule (PSA-NCAM), a molecular plasticity marker, was increased in the hippocampus of chronically isolated rats, while subsequent treatment with fluoxetine set it at the control level. In addition, analysis of cytoplasm/mitochondria redistribution of apoptotic proteins Bax and Bcl-2 after exposure to chronic isolation stress, revealed an increase in Bcl-2 protein expression in both compartments, while fluoxetine enhanced the effect of stress only in the mitochondria. The observed alterations at the molecular level were accompanied by normalization of stress-induced behavioral changes by fluoxetine. (C) 2011 Elsevier Inc. All rights reserved.
T2  - Progress in Neuro-psychopharmacology and Biological Psychiatry
T1  - Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats
VL  - 36
IS  - 1
SP  - 92
EP  - 100
DO  - 10.1016/j.pnpbp.2011.10.006
ER  - 
@article{
author = "Đorđević, Ana D. and Đorđević, Jelena D. and Elakovic, Ivana and Adžić, Miroslav and Matić, Gordana and Radoičić, Marija B.",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4678",
abstract = "Plastic response and successful adaptation to stress are of particular importance in the hippocampus, where chronic stress may cause cell death instead of neural remodeling. Structural modifications that occur both in the brain of depressed patients and animal stress models may be reversed by antidepressants. Since morphological changes induced by stress and/or antidepressants could be mediated by presynaptically located proteins, determining the levels of these proteins may be a useful way to identify molecular changes associated with synaptic plasticity. In this study we analyzed the effects of chronic (six-week) social isolation and long-term (three-week) fluoxetine treatment on molecular markers of plasticity and apoptosis in the hippocampus of Wistar rats. Compartmental redistribution of NF kappa B transcription factor involved in the regulation of plasticity and apoptosis was also examined. To establish whether social isolation is able to evoke behavioral-like effects, which might be related to the observed molecular changes, we performed the forced swimming test. The results show that synaptosomal polysialic neural cell adhesion molecule (PSA-NCAM), a molecular plasticity marker, was increased in the hippocampus of chronically isolated rats, while subsequent treatment with fluoxetine set it at the control level. In addition, analysis of cytoplasm/mitochondria redistribution of apoptotic proteins Bax and Bcl-2 after exposure to chronic isolation stress, revealed an increase in Bcl-2 protein expression in both compartments, while fluoxetine enhanced the effect of stress only in the mitochondria. The observed alterations at the molecular level were accompanied by normalization of stress-induced behavioral changes by fluoxetine. (C) 2011 Elsevier Inc. All rights reserved.",
journal = "Progress in Neuro-psychopharmacology and Biological Psychiatry",
title = "Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats",
volume = "36",
number = "1",
pages = "92-100",
doi = "10.1016/j.pnpbp.2011.10.006"
}
Đorđević, A. D., Đorđević, J. D., Elakovic, I., Adžić, M., Matić, G.,& Radoičić, M. B. (2012). Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats.
Progress in Neuro-psychopharmacology and Biological Psychiatry, 36(1), 92-100.
https://doi.org/10.1016/j.pnpbp.2011.10.006
Đorđević AD, Đorđević JD, Elakovic I, Adžić M, Matić G, Radoičić MB. Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats. Progress in Neuro-psychopharmacology and Biological Psychiatry. 2012;36(1):92-100
Đorđević Ana D., Đorđević Jelena D., Elakovic Ivana, Adžić Miroslav, Matić Gordana, Radoičić Marija B., "Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats" Progress in Neuro-psychopharmacology and Biological Psychiatry, 36, no. 1 (2012):92-100,
https://doi.org/10.1016/j.pnpbp.2011.10.006 .
41
38
39

Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers

Đorđević, Jelena D.; Đorđević, Ana D.; Adžić, Miroslav; Radoičić, Marija B.

(2012)

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Radoičić, Marija B.
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4995
AB  - Chronic stress is a contributing risk factor in the development of psychiatric illnesses, including depressive disorders. The mechanisms of their psychopathology are multifaceted and include, besides others, alterations in the brain plasticity. Previously, we investigated the effects of chronic social stress in the limbic brain structures of Wistar rats (hippocampus, HIPPO, and prefrontal cortex, PFC) and found multiple characteristics that resembled alterations described in some clinical studies of depression. We extended our investigations and followed the behavior of stressed animals by the open field test (OFT) and forced swimming test (FST), and the expression and polysialylation of synaptic plasticity markers, neural cell adhesion molecule (NCAM) and L1, in the HIPPO and PFC. We also determined the adrenal gland mass and plasma corticosterone (CORT) as a terminal part of the hypothalamic-pituitary-adrenal axis activity. Our data indicated that stressed animals avoided the central zone in the OFT and displayed decreased swimming, but prolonged immobility in the FST. The animals exhibited marked hypertrophy of the adrenal gland cortex, in spite of decreased serum CORT. Simultaneously, the stressed animals exhibited an increase in NCAM mRNA expression in the HIPPO, but not in the PFC. The synaptosomal NCAM of the HIPPO was markedly polysialylated, while cortical PSA-NCAM was significantly decreased. The results showed that chronic social isolation of Wistar rats causes both anxiety-like and depression-like behavior. These alterations are parallel with molecular changes in the limbic brain, including diminished NCAM sialylation in the PFC. Together with our previous results, the current observations suggest that a chronic social isolation model may potentially be used to study molecular mechanisms that underlie depressive symptomatology. Copyright (c) 2012 S. Karger AG, Basel
T2  - Neuropsychobiology
T1  - Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers
VL  - 66
IS  - 2
SP  - 112
EP  - 119
DO  - 10.1159/000338605
ER  - 
@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Radoičić, Marija B.",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4995",
abstract = "Chronic stress is a contributing risk factor in the development of psychiatric illnesses, including depressive disorders. The mechanisms of their psychopathology are multifaceted and include, besides others, alterations in the brain plasticity. Previously, we investigated the effects of chronic social stress in the limbic brain structures of Wistar rats (hippocampus, HIPPO, and prefrontal cortex, PFC) and found multiple characteristics that resembled alterations described in some clinical studies of depression. We extended our investigations and followed the behavior of stressed animals by the open field test (OFT) and forced swimming test (FST), and the expression and polysialylation of synaptic plasticity markers, neural cell adhesion molecule (NCAM) and L1, in the HIPPO and PFC. We also determined the adrenal gland mass and plasma corticosterone (CORT) as a terminal part of the hypothalamic-pituitary-adrenal axis activity. Our data indicated that stressed animals avoided the central zone in the OFT and displayed decreased swimming, but prolonged immobility in the FST. The animals exhibited marked hypertrophy of the adrenal gland cortex, in spite of decreased serum CORT. Simultaneously, the stressed animals exhibited an increase in NCAM mRNA expression in the HIPPO, but not in the PFC. The synaptosomal NCAM of the HIPPO was markedly polysialylated, while cortical PSA-NCAM was significantly decreased. The results showed that chronic social isolation of Wistar rats causes both anxiety-like and depression-like behavior. These alterations are parallel with molecular changes in the limbic brain, including diminished NCAM sialylation in the PFC. Together with our previous results, the current observations suggest that a chronic social isolation model may potentially be used to study molecular mechanisms that underlie depressive symptomatology. Copyright (c) 2012 S. Karger AG, Basel",
journal = "Neuropsychobiology",
title = "Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers",
volume = "66",
number = "2",
pages = "112-119",
doi = "10.1159/000338605"
}
Đorđević, J. D., Đorđević, A. D., Adžić, M.,& Radoičić, M. B. (2012). Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers.
Neuropsychobiology, 66(2), 112-119.
https://doi.org/10.1159/000338605
Đorđević JD, Đorđević AD, Adžić M, Radoičić MB. Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers. Neuropsychobiology. 2012;66(2):112-119
Đorđević Jelena D., Đorđević Ana D., Adžić Miroslav, Radoičić Marija B., "Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers" Neuropsychobiology, 66, no. 2 (2012):112-119,
https://doi.org/10.1159/000338605 .
60
47
59

Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex

Đorđević, Ana D.; Đorđević, Jelena D.; Elakovic, Ivana; Adžić, Miroslav; Matić, Gordana; Radoičić, Marija B.

(2012)

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Elakovic, Ivana
AU  - Adžić, Miroslav
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5042
AB  - The prefrontal cortex is the brain region sensitive to detrimental effects of stress and even mild stress can rapidly impair its function. Aside from initiating proadaptive neuroplastic changes in the prefrontal cortex, chronic stress may also increase vulnerability of cortical neurons to apoptosis. Understanding the mechanism of plasticity and apoptotic processes is of immense importance for therapy of stress-related psychiatric disorders. In this study we tested whether molecular alterations in the prefrontal cortex, which occurred upon chronic social isolation, could be influenced by a prolonged fluoxetine treatment. We analyzed the expression of synaptic plasticity and apoptotic molecular markers in the prefrontal cortex of young-adult male Wistar rats exposed to 6-week social isolation with and without fluoxetine treatment during the last 3 weeks. Compartmental redistribution of NF kappa B transcription factor, involved in regulation of plasticity and apoptosis, was also examined. The level of synaptosomal polysialic neural cell adhesion molecule(PSA-NCAM) was increased in the prefrontal cortex of isolated rats as compared to untreated controls. Treatment with fluoxetine reduced the PSA-NCAM level only in isolated animals. In addition, mitochondrial Bax protein was elevated by chronic social isolation, while fluoxetine failed to abolish this effect. Inspite of elevated Bcl-2 in the mitochondria, the calculated Bax/Bcl-2 ratio and concomitant absence of NF kappa B activation pointed to initiation of apoptotic signaling in the prefrontal cortex. The result simply that fluoxetine influences plasticity in the prefrontal cortex of chronically isolated rats and fails to prevent stress-induced initiation of apoptosis in this brain structure. (c) 2012 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex
VL  - 693
IS  - 1-3
SP  - 37
EP  - 44
DO  - 10.1016/j.ejphar.2012.07.042
ER  - 
@article{
author = "Đorđević, Ana D. and Đorđević, Jelena D. and Elakovic, Ivana and Adžić, Miroslav and Matić, Gordana and Radoičić, Marija B.",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5042",
abstract = "The prefrontal cortex is the brain region sensitive to detrimental effects of stress and even mild stress can rapidly impair its function. Aside from initiating proadaptive neuroplastic changes in the prefrontal cortex, chronic stress may also increase vulnerability of cortical neurons to apoptosis. Understanding the mechanism of plasticity and apoptotic processes is of immense importance for therapy of stress-related psychiatric disorders. In this study we tested whether molecular alterations in the prefrontal cortex, which occurred upon chronic social isolation, could be influenced by a prolonged fluoxetine treatment. We analyzed the expression of synaptic plasticity and apoptotic molecular markers in the prefrontal cortex of young-adult male Wistar rats exposed to 6-week social isolation with and without fluoxetine treatment during the last 3 weeks. Compartmental redistribution of NF kappa B transcription factor, involved in regulation of plasticity and apoptosis, was also examined. The level of synaptosomal polysialic neural cell adhesion molecule(PSA-NCAM) was increased in the prefrontal cortex of isolated rats as compared to untreated controls. Treatment with fluoxetine reduced the PSA-NCAM level only in isolated animals. In addition, mitochondrial Bax protein was elevated by chronic social isolation, while fluoxetine failed to abolish this effect. Inspite of elevated Bcl-2 in the mitochondria, the calculated Bax/Bcl-2 ratio and concomitant absence of NF kappa B activation pointed to initiation of apoptotic signaling in the prefrontal cortex. The result simply that fluoxetine influences plasticity in the prefrontal cortex of chronically isolated rats and fails to prevent stress-induced initiation of apoptosis in this brain structure. (c) 2012 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex",
volume = "693",
number = "1-3",
pages = "37-44",
doi = "10.1016/j.ejphar.2012.07.042"
}
Đorđević, A. D., Đorđević, J. D., Elakovic, I., Adžić, M., Matić, G.,& Radoičić, M. B. (2012). Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex.
European Journal of Pharmacology, 693(1-3), 37-44.
https://doi.org/10.1016/j.ejphar.2012.07.042
Đorđević AD, Đorđević JD, Elakovic I, Adžić M, Matić G, Radoičić MB. Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex. European Journal of Pharmacology. 2012;693(1-3):37-44
Đorđević Ana D., Đorđević Jelena D., Elakovic Ivana, Adžić Miroslav, Matić Gordana, Radoičić Marija B., "Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex" European Journal of Pharmacology, 693, no. 1-3 (2012):37-44,
https://doi.org/10.1016/j.ejphar.2012.07.042 .
17
18
19

Matrix metalloproteinase-1 promoter genotypes and haplotypes are associated with carotid plaque presence

Đurić, Tamara; Stojković, Ljiljana S.; Živković, Maja; Končar, Igor; Stanković, Aleksandra; Đorđević, Ana D.; Alavantić, Dragan

(2012)

TY  - JOUR
AU  - Đurić, Tamara
AU  - Stojković, Ljiljana S.
AU  - Živković, Maja
AU  - Končar, Igor
AU  - Stanković, Aleksandra
AU  - Đorđević, Ana D.
AU  - Alavantić, Dragan
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5161
AB  - Objectives: Matrix metalloproteinase (MMP)-1 degrades fibrillar collagens suggesting important role in vascular remodeling. Data about MMP-1 promoter polymorphisms and carotid atherosclerosis (CA) are scarce. The aim of this study was to evaluate association of MMP-1 genotypes/haplotypes with carotid plaque (CP) presence in Serbian population. Design and methods: Study enrolled a total of 702 participants: 274 controls and 428 consecutive patients with CA who underwent carotid endarterectomy. MMP-1 polymorphisms -1607 1G/2G, -519 A/G and -340 T/C were genotyped by PCR and RFLP methods. Results: Individuals carrying MMP-1 - 1607 2G allele had significantly increased allele dose-dependent risk for CP presence (1G1G vs. 1G2G vs. 2G2G; OR = 1; OR = 1.87 95% CI 1.29-2.07; OR= 3.49 95% CI 1.67-7.30. p = 0.0009, respectively). Compared to the referent haplotype 2G_ (1607)-T_ (340)-A_(519), the haplotypes 1G_(1607)-T_(340)-A_(519), 1G-(1607)-T_(340)-G_519 and 2G_(1607)-C_(340)-A_(519) had statistically significant protective effect on CP presence (OR = 0.41, 95% CI 0.29-0.81, p = 0.01; OR = 0.56, 95% CI 0.44-0.89, p = 0.01: OR = 0.43, 95% CI 0.27-0.86, p = 0.02, respectively). Conclusions: MMP-1 - 1607 G/2G polymorphism solely and specific haplotypes of three analyzed promoter polymorphisms are significantly and independently associated with occurrence of CP. Replication studies in other populations are needed. (c) 2012 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
T2  - Clinical Biochemistry
T1  - Matrix metalloproteinase-1 promoter genotypes and haplotypes are associated with carotid plaque presence
VL  - 45
IS  - 16-17
SP  - 1353
EP  - 1356
DO  - 10.1016/j.clinbiochem.2012.05.032
ER  - 
@article{
author = "Đurić, Tamara and Stojković, Ljiljana S. and Živković, Maja and Končar, Igor and Stanković, Aleksandra and Đorđević, Ana D. and Alavantić, Dragan",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5161",
abstract = "Objectives: Matrix metalloproteinase (MMP)-1 degrades fibrillar collagens suggesting important role in vascular remodeling. Data about MMP-1 promoter polymorphisms and carotid atherosclerosis (CA) are scarce. The aim of this study was to evaluate association of MMP-1 genotypes/haplotypes with carotid plaque (CP) presence in Serbian population. Design and methods: Study enrolled a total of 702 participants: 274 controls and 428 consecutive patients with CA who underwent carotid endarterectomy. MMP-1 polymorphisms -1607 1G/2G, -519 A/G and -340 T/C were genotyped by PCR and RFLP methods. Results: Individuals carrying MMP-1 - 1607 2G allele had significantly increased allele dose-dependent risk for CP presence (1G1G vs. 1G2G vs. 2G2G; OR = 1; OR = 1.87 95% CI 1.29-2.07; OR= 3.49 95% CI 1.67-7.30. p = 0.0009, respectively). Compared to the referent haplotype 2G_ (1607)-T_ (340)-A_(519), the haplotypes 1G_(1607)-T_(340)-A_(519), 1G-(1607)-T_(340)-G_519 and 2G_(1607)-C_(340)-A_(519) had statistically significant protective effect on CP presence (OR = 0.41, 95% CI 0.29-0.81, p = 0.01; OR = 0.56, 95% CI 0.44-0.89, p = 0.01: OR = 0.43, 95% CI 0.27-0.86, p = 0.02, respectively). Conclusions: MMP-1 - 1607 G/2G polymorphism solely and specific haplotypes of three analyzed promoter polymorphisms are significantly and independently associated with occurrence of CP. Replication studies in other populations are needed. (c) 2012 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.",
journal = "Clinical Biochemistry",
title = "Matrix metalloproteinase-1 promoter genotypes and haplotypes are associated with carotid plaque presence",
volume = "45",
number = "16-17",
pages = "1353-1356",
doi = "10.1016/j.clinbiochem.2012.05.032"
}
Đurić, T., Stojković, L. S., Živković, M., Končar, I., Stanković, A., Đorđević, A. D.,& Alavantić, D. (2012). Matrix metalloproteinase-1 promoter genotypes and haplotypes are associated with carotid plaque presence.
Clinical Biochemistry, 45(16-17), 1353-1356.
https://doi.org/10.1016/j.clinbiochem.2012.05.032
Đurić T, Stojković LS, Živković M, Končar I, Stanković A, Đorđević AD, Alavantić D. Matrix metalloproteinase-1 promoter genotypes and haplotypes are associated with carotid plaque presence. Clinical Biochemistry. 2012;45(16-17):1353-1356
Đurić Tamara, Stojković Ljiljana S., Živković Maja, Končar Igor, Stanković Aleksandra, Đorđević Ana D., Alavantić Dragan, "Matrix metalloproteinase-1 promoter genotypes and haplotypes are associated with carotid plaque presence" Clinical Biochemistry, 45, no. 16-17 (2012):1353-1356,
https://doi.org/10.1016/j.clinbiochem.2012.05.032 .
14
13
13

Gender-specific response of brain corticosteroid receptors to stress and fluoxetine

Elakovic, Ivana; Đorđević, Ana D.; Adžić, Miroslav; Đorđević, Jelena D.; Radoičić, Marija B.; Matić, Gordana

(2011)

TY  - JOUR
AU  - Elakovic, Ivana
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Radoičić, Marija B.
AU  - Matić, Gordana
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4277
AB  - Gender-related differences in dexamethasone binding to corticosteroid receptors (CR) and in glucocorticoid receptor (GR) protein level in the pituitary, hypothalamus, hippocampus and prefrontal cortex were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Untreated males, in comparison to females, displayed higher hormone-binding capacity of both GR and mineralocorticoid receptor (MR) in the hippocampal cytosol, as well as higher GR protein level in the pituitary cytosol. In both genders, dexamethasone binding to MR exceeded that to GR. While fluoxetine treatment and social isolation had no effect on GR activity, the influence on MR was gender-specific. Fluoxetine facilitated MR hormone-binding only in females, increasing the MR/GA activity ratio. In contrast, after a 6-week isolation of males, MR binding capacity was diminished and MR/GR ratio inverted in favor of GR In addition, fluoxetine induced elevation of cytosolic GR protein level in the pituitary and hypothalamus, the latter change being gender-specific. The results point to gender-related differences in the CRs functioning and suggest that both MR and GR may contribute to well-known sexual dimorphism in vulnerability to stress and stress-related disorders and in the outcome of antidepressant treatment. (C) 2011 Elsevier B.V. All rights reserved.
T2  - Brain Research
T1  - Gender-specific response of brain corticosteroid receptors to stress and fluoxetine
VL  - 1384
SP  - 61
EP  - 68
DO  - 10.1016/j.brainres.2011.01.078
ER  - 
@article{
author = "Elakovic, Ivana and Đorđević, Ana D. and Adžić, Miroslav and Đorđević, Jelena D. and Radoičić, Marija B. and Matić, Gordana",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4277",
abstract = "Gender-related differences in dexamethasone binding to corticosteroid receptors (CR) and in glucocorticoid receptor (GR) protein level in the pituitary, hypothalamus, hippocampus and prefrontal cortex were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Untreated males, in comparison to females, displayed higher hormone-binding capacity of both GR and mineralocorticoid receptor (MR) in the hippocampal cytosol, as well as higher GR protein level in the pituitary cytosol. In both genders, dexamethasone binding to MR exceeded that to GR. While fluoxetine treatment and social isolation had no effect on GR activity, the influence on MR was gender-specific. Fluoxetine facilitated MR hormone-binding only in females, increasing the MR/GA activity ratio. In contrast, after a 6-week isolation of males, MR binding capacity was diminished and MR/GR ratio inverted in favor of GR In addition, fluoxetine induced elevation of cytosolic GR protein level in the pituitary and hypothalamus, the latter change being gender-specific. The results point to gender-related differences in the CRs functioning and suggest that both MR and GR may contribute to well-known sexual dimorphism in vulnerability to stress and stress-related disorders and in the outcome of antidepressant treatment. (C) 2011 Elsevier B.V. All rights reserved.",
journal = "Brain Research",
title = "Gender-specific response of brain corticosteroid receptors to stress and fluoxetine",
volume = "1384",
pages = "61-68",
doi = "10.1016/j.brainres.2011.01.078"
}
Elakovic, I., Đorđević, A. D., Adžić, M., Đorđević, J. D., Radoičić, M. B.,& Matić, G. (2011). Gender-specific response of brain corticosteroid receptors to stress and fluoxetine.
Brain Research, 1384, 61-68.
https://doi.org/10.1016/j.brainres.2011.01.078
Elakovic I, Đorđević AD, Adžić M, Đorđević JD, Radoičić MB, Matić G. Gender-specific response of brain corticosteroid receptors to stress and fluoxetine. Brain Research. 2011;1384:61-68
Elakovic Ivana, Đorđević Ana D., Adžić Miroslav, Đorđević Jelena D., Radoičić Marija B., Matić Gordana, "Gender-specific response of brain corticosteroid receptors to stress and fluoxetine" Brain Research, 1384 (2011):61-68,
https://doi.org/10.1016/j.brainres.2011.01.078 .
17
16
16

Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver

Đorđević, Jelena D.; Đorđević, Ana D.; Adžić, Miroslav; Elakovic, Ivana; Matić, Gordana; Radoičić, Marija B.

(2011)

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Elakovic, Ivana
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4329
AB  - Selective serotonin reuptake inhibitors (SSRI) are a treatment of choice for stress related disorders including clinical depression and a range of anxiety-related disorders. In the experimental animals, chronic stress paradigms are considered as a model of depression, and in that context are used for examining the effects of different drug treatments. The present research was designed to investigate the effect of SSRI fluoxetine on antioxidant status and apoptotic signaling in Wistar rat liver, which is a central organ for activation and detoxification of many xenobiotics and reactive oxygen species. We also investigated whether chronic fluoxetine treatment exhibits the same effects in the liver of control animals vs. animals stressed by chronic psychosocial isolation. Our results revealed that fluoxetine downregulated the activity of superoxide dismutases and upregulated the activity of glutathione peroxidase in both rat groups, while elevating glutathione reductase activity and total antioxidant status only in stressed animals. These results suggested that fluoxetine interfered with stress-induced pathways of oxidative defense in the liver. In addition, in both experimental groups, fluoxetine induced several hallmarks of apoptosis in the liver, including a decrease in Bcl-2 expression and increased DNA fragmentation. However, apoptotic alterations were more pronounced in stressed animals, suggesting that stress related oxidative damage could have primed apoptotic effects of fluoxetine. (C) 2011 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver
VL  - 659
IS  - 1
SP  - 61
EP  - 66
DO  - 10.1016/j.ejphar.2011.03.003
ER  - 
@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Elakovic, Ivana and Matić, Gordana and Radoičić, Marija B.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4329",
abstract = "Selective serotonin reuptake inhibitors (SSRI) are a treatment of choice for stress related disorders including clinical depression and a range of anxiety-related disorders. In the experimental animals, chronic stress paradigms are considered as a model of depression, and in that context are used for examining the effects of different drug treatments. The present research was designed to investigate the effect of SSRI fluoxetine on antioxidant status and apoptotic signaling in Wistar rat liver, which is a central organ for activation and detoxification of many xenobiotics and reactive oxygen species. We also investigated whether chronic fluoxetine treatment exhibits the same effects in the liver of control animals vs. animals stressed by chronic psychosocial isolation. Our results revealed that fluoxetine downregulated the activity of superoxide dismutases and upregulated the activity of glutathione peroxidase in both rat groups, while elevating glutathione reductase activity and total antioxidant status only in stressed animals. These results suggested that fluoxetine interfered with stress-induced pathways of oxidative defense in the liver. In addition, in both experimental groups, fluoxetine induced several hallmarks of apoptosis in the liver, including a decrease in Bcl-2 expression and increased DNA fragmentation. However, apoptotic alterations were more pronounced in stressed animals, suggesting that stress related oxidative damage could have primed apoptotic effects of fluoxetine. (C) 2011 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver",
volume = "659",
number = "1",
pages = "61-66",
doi = "10.1016/j.ejphar.2011.03.003"
}
Đorđević, J. D., Đorđević, A. D., Adžić, M., Elakovic, I., Matić, G.,& Radoičić, M. B. (2011). Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver.
European Journal of Pharmacology, 659(1), 61-66.
https://doi.org/10.1016/j.ejphar.2011.03.003
Đorđević JD, Đorđević AD, Adžić M, Elakovic I, Matić G, Radoičić MB. Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver. European Journal of Pharmacology. 2011;659(1):61-66
Đorđević Jelena D., Đorđević Ana D., Adžić Miroslav, Elakovic Ivana, Matić Gordana, Radoičić Marija B., "Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver" European Journal of Pharmacology, 659, no. 1 (2011):61-66,
https://doi.org/10.1016/j.ejphar.2011.03.003 .
46
39
46

Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats

Adžić, Miroslav; Đorđević, Jelena D.; Mitić, Miloš; Simić, Iva; Rackov, Gorjana; Đorđević, Ana D.; Elakovic, Ivana; Matić, Gordana; Radoičić, Marija B.

(2011)

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Mitić, Miloš
AU  - Simić, Iva
AU  - Rackov, Gorjana
AU  - Đorđević, Ana D.
AU  - Elakovic, Ivana
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4640
AB  - Alterations in the antioxidative defense parameters upon chronic stress are considered critical for pathophysiology of stress related psychiatric disorders, and their status in blood serves as biomarker for effects of pharmacological treatments. The present study was designed to investigate the modulation of erythrocyte antioxidant enzymes (AOEs): CuZn superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR) activities and their protein expression in Wistar male rats subjected to chronic psychosocial isolation and/or to pharmacological treatment with fluoxetine. Chronically isolated animals exhibited decreased levels of serum corticosterone, as opposed to other chronic stress paradigms. In addition to that, SOD, CAT and GPx status was not altered either by chronic psychosocial isolation or by fluoxetine treatment. In contrast, GLR activity and its protein level were both markedly reduced by fluoxetine. Since, GLR is crucial for overall oxido-reductive balance through maintaining optimal ratio of reduced/oxidized glutathione level (GSH/GSSG) in erythrocytes, these results could indicate that in spite of numerous beneficial effects of fluoxetine, it may compromise both haemoglobin function and oxygen transport.
T2  - Acta Chimica Slovenica
T1  - Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats
VL  - 58
IS  - 4
SP  - 785
EP  - 791
ER  - 
@article{
author = "Adžić, Miroslav and Đorđević, Jelena D. and Mitić, Miloš and Simić, Iva and Rackov, Gorjana and Đorđević, Ana D. and Elakovic, Ivana and Matić, Gordana and Radoičić, Marija B.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4640",
abstract = "Alterations in the antioxidative defense parameters upon chronic stress are considered critical for pathophysiology of stress related psychiatric disorders, and their status in blood serves as biomarker for effects of pharmacological treatments. The present study was designed to investigate the modulation of erythrocyte antioxidant enzymes (AOEs): CuZn superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR) activities and their protein expression in Wistar male rats subjected to chronic psychosocial isolation and/or to pharmacological treatment with fluoxetine. Chronically isolated animals exhibited decreased levels of serum corticosterone, as opposed to other chronic stress paradigms. In addition to that, SOD, CAT and GPx status was not altered either by chronic psychosocial isolation or by fluoxetine treatment. In contrast, GLR activity and its protein level were both markedly reduced by fluoxetine. Since, GLR is crucial for overall oxido-reductive balance through maintaining optimal ratio of reduced/oxidized glutathione level (GSH/GSSG) in erythrocytes, these results could indicate that in spite of numerous beneficial effects of fluoxetine, it may compromise both haemoglobin function and oxygen transport.",
journal = "Acta Chimica Slovenica",
title = "Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats",
volume = "58",
number = "4",
pages = "785-791"
}
Adžić, M., Đorđević, J. D., Mitić, M., Simić, I., Rackov, G., Đorđević, A. D., Elakovic, I., Matić, G.,& Radoičić, M. B. (2011). Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats.
Acta Chimica Slovenica, 58(4), 785-791.
Adžić M, Đorđević JD, Mitić M, Simić I, Rackov G, Đorđević AD, Elakovic I, Matić G, Radoičić MB. Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats. Acta Chimica Slovenica. 2011;58(4):785-791
Adžić Miroslav, Đorđević Jelena D., Mitić Miloš, Simić Iva, Rackov Gorjana, Đorđević Ana D., Elakovic Ivana, Matić Gordana, Radoičić Marija B., "Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats" Acta Chimica Slovenica, 58, no. 4 (2011):785-791
4

Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine

Elakovic, Ivana; Vasiljevic, Dorde; Adžić, Miroslav; Đorđević, Ana D.; Đorđević, Jelena D.; Radoičić, Marija B.; Matić, Gordana

(2010)

TY  - JOUR
AU  - Elakovic, Ivana
AU  - Vasiljevic, Dorde
AU  - Adžić, Miroslav
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Radoičić, Marija B.
AU  - Matić, Gordana
PY  - 2010
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3960
AB  - Gender-related differences in the expression and functional properties of the hepatic glucocorticoid receptor were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Some of the receptors functional properties, including hormone-binding capacity (B-max), hormone-binding potency (B-max/K-D ratio) and the DNA-binding ability, were found to be sexually dimorphic. Fluoxetine treatment (5 mg/kg body mass, 21 day, intraperitoneally) induced a decrease in B-max and in the amount of Hsp70 co-immunoprecipitated with the glucocorticoid receptor only in males, and stimulated the association of the receptor with Hsp90 in females. When applied during the last three weeks of the 6-week isolation, fluoxetine parallelly elevated B-max and the receptor protein level in female animals, while in males diminished B-max and inhibited association of the receptor with Hsp70. Binding of dexamethasone-receptor complexes both to DNA-cellulose and to isolated liver nuclei did not appear to be a target for fluoxetine action. The results point to sex-related differences in the glucocorticoid receptor functioning and in its response to fluoxetine, and suggest that these differences may contribute to well known sexual dimorphism in the sensitivity to stress, to stress-related disorders and to antidepressant treatment. (C) 2010 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine
VL  - 632
IS  - 1-3
SP  - 79
EP  - 85
DO  - 10.1016/j.ejphar.2010.01.015
ER  - 
@article{
author = "Elakovic, Ivana and Vasiljevic, Dorde and Adžić, Miroslav and Đorđević, Ana D. and Đorđević, Jelena D. and Radoičić, Marija B. and Matić, Gordana",
year = "2010",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3960",
abstract = "Gender-related differences in the expression and functional properties of the hepatic glucocorticoid receptor were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Some of the receptors functional properties, including hormone-binding capacity (B-max), hormone-binding potency (B-max/K-D ratio) and the DNA-binding ability, were found to be sexually dimorphic. Fluoxetine treatment (5 mg/kg body mass, 21 day, intraperitoneally) induced a decrease in B-max and in the amount of Hsp70 co-immunoprecipitated with the glucocorticoid receptor only in males, and stimulated the association of the receptor with Hsp90 in females. When applied during the last three weeks of the 6-week isolation, fluoxetine parallelly elevated B-max and the receptor protein level in female animals, while in males diminished B-max and inhibited association of the receptor with Hsp70. Binding of dexamethasone-receptor complexes both to DNA-cellulose and to isolated liver nuclei did not appear to be a target for fluoxetine action. The results point to sex-related differences in the glucocorticoid receptor functioning and in its response to fluoxetine, and suggest that these differences may contribute to well known sexual dimorphism in the sensitivity to stress, to stress-related disorders and to antidepressant treatment. (C) 2010 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine",
volume = "632",
number = "1-3",
pages = "79-85",
doi = "10.1016/j.ejphar.2010.01.015"
}
Elakovic, I., Vasiljevic, D., Adžić, M., Đorđević, A. D., Đorđević, J. D., Radoičić, M. B.,& Matić, G. (2010). Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine.
European Journal of Pharmacology, 632(1-3), 79-85.
https://doi.org/10.1016/j.ejphar.2010.01.015
Elakovic I, Vasiljevic D, Adžić M, Đorđević AD, Đorđević JD, Radoičić MB, Matić G. Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine. European Journal of Pharmacology. 2010;632(1-3):79-85
Elakovic Ivana, Vasiljevic Dorde, Adžić Miroslav, Đorđević Ana D., Đorđević Jelena D., Radoičić Marija B., Matić Gordana, "Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine" European Journal of Pharmacology, 632, no. 1-3 (2010):79-85,
https://doi.org/10.1016/j.ejphar.2010.01.015 .
8
8
8

Chronic Social Isolation Compromises the Activity of Both Glutathione Peroxidase and Catalase in Hippocampus of Male Wistar Rats

Đorđević, Jelena D.; Đorđević, Ana D.; Adžić, Miroslav; Radoičić, Marija B.

(2010)

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Radoičić, Marija B.
PY  - 2010
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4020
AB  - Chronic neuroendocrine stress usually leads to the elevation of the stress hormones and increased metabolic rate, which is frequently accompanied by oxidative damage to the CNS. In the present study we hypothesized that chronic psychosocial isolation (CPSI) of male Wistar rats, characterized by decreased serum corticosterone (CORT), unaltered catecholamines (CTs), and low blood glucose (GLU), may also promote oxidative imbalance in the CNS, by targeting antioxidant defense system. To test it, we have examined the relation between these input signals and protein expression/activity of antioxidant enzymes (AOEs): superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GLR) in the hippocampus (HIPPO) of CPSI animals. We found that CPSI did not affect SODs or CAT, but decreased activity of GPx and compromised GLR, an enzyme highly dependent on blood GLU for its substrate precursor. Further, we have tested whether the CPSI experience altered AOEs response to a novelty stress, and found that it attenuated peroxide-metabolizing enzymes, CAT and GPx, and decreased GLR activity, even though blood GLU was restored. The altered ratios of hippocampal AOEs in CPSI animals, which were worsened under the combined stress conditions, may lead to the accumulation of peroxide products and oxidative imbalance. The mechanism by which CPSI generate oxidative imbalance in the HIPPO is most likely based on poor systemic energy conditions set by this stress. Such conditions may cause functional decline of CNS structures, such as HIPPO, and are likely to promote state linked to onset of many mood disorders.
T2  - Cellular and Molecular Neurobiology
T1  - Chronic Social Isolation Compromises the Activity of Both Glutathione Peroxidase and Catalase in Hippocampus of Male Wistar Rats
VL  - 30
IS  - 5
SP  - 693
EP  - 700
DO  - 10.1007/s10571-009-9493-0
ER  - 
@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Radoičić, Marija B.",
year = "2010",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4020",
abstract = "Chronic neuroendocrine stress usually leads to the elevation of the stress hormones and increased metabolic rate, which is frequently accompanied by oxidative damage to the CNS. In the present study we hypothesized that chronic psychosocial isolation (CPSI) of male Wistar rats, characterized by decreased serum corticosterone (CORT), unaltered catecholamines (CTs), and low blood glucose (GLU), may also promote oxidative imbalance in the CNS, by targeting antioxidant defense system. To test it, we have examined the relation between these input signals and protein expression/activity of antioxidant enzymes (AOEs): superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GLR) in the hippocampus (HIPPO) of CPSI animals. We found that CPSI did not affect SODs or CAT, but decreased activity of GPx and compromised GLR, an enzyme highly dependent on blood GLU for its substrate precursor. Further, we have tested whether the CPSI experience altered AOEs response to a novelty stress, and found that it attenuated peroxide-metabolizing enzymes, CAT and GPx, and decreased GLR activity, even though blood GLU was restored. The altered ratios of hippocampal AOEs in CPSI animals, which were worsened under the combined stress conditions, may lead to the accumulation of peroxide products and oxidative imbalance. The mechanism by which CPSI generate oxidative imbalance in the HIPPO is most likely based on poor systemic energy conditions set by this stress. Such conditions may cause functional decline of CNS structures, such as HIPPO, and are likely to promote state linked to onset of many mood disorders.",
journal = "Cellular and Molecular Neurobiology",
title = "Chronic Social Isolation Compromises the Activity of Both Glutathione Peroxidase and Catalase in Hippocampus of Male Wistar Rats",
volume = "30",
number = "5",
pages = "693-700",
doi = "10.1007/s10571-009-9493-0"
}
Đorđević, J. D., Đorđević, A. D., Adžić, M.,& Radoičić, M. B. (2010). Chronic Social Isolation Compromises the Activity of Both Glutathione Peroxidase and Catalase in Hippocampus of Male Wistar Rats.
Cellular and Molecular Neurobiology, 30(5), 693-700.
https://doi.org/10.1007/s10571-009-9493-0
Đorđević JD, Đorđević AD, Adžić M, Radoičić MB. Chronic Social Isolation Compromises the Activity of Both Glutathione Peroxidase and Catalase in Hippocampus of Male Wistar Rats. Cellular and Molecular Neurobiology. 2010;30(5):693-700
Đorđević Jelena D., Đorđević Ana D., Adžić Miroslav, Radoičić Marija B., "Chronic Social Isolation Compromises the Activity of Both Glutathione Peroxidase and Catalase in Hippocampus of Male Wistar Rats" Cellular and Molecular Neurobiology, 30, no. 5 (2010):693-700,
https://doi.org/10.1007/s10571-009-9493-0 .
24
21
23

Chronic Social Isolation Suppresses Proplastic Response and Promotes Proapoptotic Signalling in Prefrontal Cortex of Wistar Rats

Đorđević, Ana D.; Adžić, Miroslav; Đorđević, Jelena D.; Radoičić, Marija B.

(2010)

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Radoičić, Marija B.
PY  - 2010
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4060
AB  - Successful adaptation to stress involves synergized actions of glucocorticoids and catecholamines at several levels of the CNS, including the prefrontal cortex (PFC). Inside the PFC, hormonal signals trigger concerted actions of transcriptional factors, such as glucocorticoid receptor (GR) and nuclear factor kappa B (NF kappa B), culminating in a balanced, proadaptive expression of their common genes, such as proplastic NCAM and/or apoptotic Bax and Bcl-2. In the present study, we hypothesized that chronic stress may compromise the balance between GR and NF kappa B signals and lead to an altered/maladaptive expression of their cognate genes in the PFC. Our results obtained with Wistar rats exposed to chronic social isolation indicated alterations of the GR relative to the NF kappa B, in favor of the GA, in both the cytoplasmic and the nuclear compartments of the PFC. Although these alterations did not affect the induction of proplastic NCAM gene, they decreased the NCAM sialylation necessary for plastic response and caused marked relocation of the mitochondrial membrane antiapoptotic Bcl-2 protein to its cytoplasmic form. Moreover, the compromised PSA-NCAM plastic response found under chronic stress was sustained after exposure of animals to the subsequent acute stress, whereas the proapoptotic signals were further emphasized. It is concluded that chronic social isolation of Wistar animals leads to a maladaptive response of the PFC, considering the diminishment of its plastic potential and potentiating of apoptosis. Such conditions in the PFC are likely to compromise its ability to interact with other CNS structures, such as the hippocampus, which is necessary for successful adaptation to stress. (C) 2010 Wiley-Liss, Inc.
T2  - Journal of Neuroscience Research
T1  - Chronic Social Isolation Suppresses Proplastic Response and Promotes Proapoptotic Signalling in Prefrontal Cortex of Wistar Rats
VL  - 88
IS  - 11
SP  - 2524
EP  - 2533
DO  - 10.1002/jnr.22403
ER  - 
@article{
author = "Đorđević, Ana D. and Adžić, Miroslav and Đorđević, Jelena D. and Radoičić, Marija B.",
year = "2010",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4060",
abstract = "Successful adaptation to stress involves synergized actions of glucocorticoids and catecholamines at several levels of the CNS, including the prefrontal cortex (PFC). Inside the PFC, hormonal signals trigger concerted actions of transcriptional factors, such as glucocorticoid receptor (GR) and nuclear factor kappa B (NF kappa B), culminating in a balanced, proadaptive expression of their common genes, such as proplastic NCAM and/or apoptotic Bax and Bcl-2. In the present study, we hypothesized that chronic stress may compromise the balance between GR and NF kappa B signals and lead to an altered/maladaptive expression of their cognate genes in the PFC. Our results obtained with Wistar rats exposed to chronic social isolation indicated alterations of the GR relative to the NF kappa B, in favor of the GA, in both the cytoplasmic and the nuclear compartments of the PFC. Although these alterations did not affect the induction of proplastic NCAM gene, they decreased the NCAM sialylation necessary for plastic response and caused marked relocation of the mitochondrial membrane antiapoptotic Bcl-2 protein to its cytoplasmic form. Moreover, the compromised PSA-NCAM plastic response found under chronic stress was sustained after exposure of animals to the subsequent acute stress, whereas the proapoptotic signals were further emphasized. It is concluded that chronic social isolation of Wistar animals leads to a maladaptive response of the PFC, considering the diminishment of its plastic potential and potentiating of apoptosis. Such conditions in the PFC are likely to compromise its ability to interact with other CNS structures, such as the hippocampus, which is necessary for successful adaptation to stress. (C) 2010 Wiley-Liss, Inc.",
journal = "Journal of Neuroscience Research",
title = "Chronic Social Isolation Suppresses Proplastic Response and Promotes Proapoptotic Signalling in Prefrontal Cortex of Wistar Rats",
volume = "88",
number = "11",
pages = "2524-2533",
doi = "10.1002/jnr.22403"
}
Đorđević, A. D., Adžić, M., Đorđević, J. D.,& Radoičić, M. B. (2010). Chronic Social Isolation Suppresses Proplastic Response and Promotes Proapoptotic Signalling in Prefrontal Cortex of Wistar Rats.
Journal of Neuroscience Research, 88(11), 2524-2533.
https://doi.org/10.1002/jnr.22403
Đorđević AD, Adžić M, Đorđević JD, Radoičić MB. Chronic Social Isolation Suppresses Proplastic Response and Promotes Proapoptotic Signalling in Prefrontal Cortex of Wistar Rats. Journal of Neuroscience Research. 2010;88(11):2524-2533
Đorđević Ana D., Adžić Miroslav, Đorđević Jelena D., Radoičić Marija B., "Chronic Social Isolation Suppresses Proplastic Response and Promotes Proapoptotic Signalling in Prefrontal Cortex of Wistar Rats" Journal of Neuroscience Research, 88, no. 11 (2010):2524-2533,
https://doi.org/10.1002/jnr.22403 .
22
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Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats

Đorđević, Jelena D.; Đorđević, Ana D.; Adžić, Miroslav; Niciforovic, A.; Radoičić, Marija B.

(2010)

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Niciforovic, A.
AU  - Radoičić, Marija B.
PY  - 2010
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4153
AB  - Clinical reports suggest close interactions between stressors, particularly those of long duration, and liver diseases, such as hepatic inflammation, that is proposed to occur via reactive oxygen species. In the present study we have used 21-day social isolation of male Wistar rats as a model of chronic stress to investigate protein expression/activity of liver antioxidant enzymes: superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR), and protein expression of their upstream regulators: glucocorticoid receptor (GR) and nuclear factor kappa B (NFkB). We have also characterized these parameters in either naive or chronically stressed animals that were challenged by 30-min acute immobilization. We found that chronic isolation caused decrease in serum corticosterone (CORT) and blood glucose (GLU), increase in NFkB signaling, and disproportion between CuZnSOD, peroxidases (CAT, GPx) and GLR, thus promoting H2O2 accumulation and prooxidative state in liver. The overall results suggested that chronic stress exaggerated responsiveness to subsequent stressor at the level of CORT and GLU, and potentiated GLR response, but compromised the restoration of oxido-reductive balance due to irreversible alterations in MnSOD and GPx.
T2  - Physiological Research
T1  - Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats
VL  - 59
IS  - 5
SP  - 729
EP  - 736
ER  - 
@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Niciforovic, A. and Radoičić, Marija B.",
year = "2010",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4153",
abstract = "Clinical reports suggest close interactions between stressors, particularly those of long duration, and liver diseases, such as hepatic inflammation, that is proposed to occur via reactive oxygen species. In the present study we have used 21-day social isolation of male Wistar rats as a model of chronic stress to investigate protein expression/activity of liver antioxidant enzymes: superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR), and protein expression of their upstream regulators: glucocorticoid receptor (GR) and nuclear factor kappa B (NFkB). We have also characterized these parameters in either naive or chronically stressed animals that were challenged by 30-min acute immobilization. We found that chronic isolation caused decrease in serum corticosterone (CORT) and blood glucose (GLU), increase in NFkB signaling, and disproportion between CuZnSOD, peroxidases (CAT, GPx) and GLR, thus promoting H2O2 accumulation and prooxidative state in liver. The overall results suggested that chronic stress exaggerated responsiveness to subsequent stressor at the level of CORT and GLU, and potentiated GLR response, but compromised the restoration of oxido-reductive balance due to irreversible alterations in MnSOD and GPx.",
journal = "Physiological Research",
title = "Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats",
volume = "59",
number = "5",
pages = "729-736"
}
Đorđević, J. D., Đorđević, A. D., Adžić, M., Niciforovic, A.,& Radoičić, M. B. (2010). Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats.
Physiological Research, 59(5), 729-736.
Đorđević JD, Đorđević AD, Adžić M, Niciforovic A, Radoičić MB. Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats. Physiological Research. 2010;59(5):729-736
Đorđević Jelena D., Đorđević Ana D., Adžić Miroslav, Niciforovic A., Radoičić Marija B., "Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats" Physiological Research, 59, no. 5 (2010):729-736
37