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Sudar-Milovanović, Emina

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Authority KeyName Variants
orcid::0000-0002-2273-5310
  • Sudar-Milovanović, Emina (14)
  • Sudar, Emina (32)
Projects
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 Carotid disease in Serbia - pathologic dynamics, prevention, diagnostics and inovative therapeutic methods
Cell Cycle Aberrations and the Impact of Oxidative Stress in Neurodegenerative Processes and Malignant Transformation of the Cell Modulation of intracellular energy balance-controlling signalling pathways in therapy of cancer and neuro-immuno-endocrine disorders
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 Clinical Center Zemun
CNRS, University Pierre and Marie Curie, Ministry of Science, Republic of Serbia [14303013], Ministry of Foreign Affairs [337-00-359/2005-01/16] CNRS, University Pierre and Marie Curie, Ministry of Science, Republic of Serbia [143030B], Pavle Savic [337-00-359/2005-01/16], Republic of France, Ministry of Foreign Affairs
The study of physicochemical and biochemical processes in living environment that have impacts on pollution and the investigation of possibilities for minimizing the consequences Application of the EIIP/ISM bioinformatics platform in discovery of novel therapeutic targets and potential therapeutic molecules
Effects of metabolic and nonmetabolic stressors on the expression and action of neuroendocrine regulators of energy homeostasis Structural characterisation of the insulin-like growth factor (IGF) binding proteins and IGF receptors, their interactions with other physiological molecules and alterations in metabolic disorders
Research of endocrine regulatory mechanisms, markers of systemic inflammation and cardiovascular risk factors in metabolic disorders Effects of modulation of biohumoral, inflammatory and metabolic response in acute ST-segment elevation myocardial infarction on survival and left ventricular function
Defining a cluster of molecular biomarkers for improved diagnostics and therapy of mood disorders Biological effects, nutritional intake and status of folate and polysaturate fatty acid (PUFA): improvement of nutrition in Serbia
KAUST Base Research Fund [BAS/1/1606‐01‐01] KAUST Base Research Funds [BAS/1/1059-01-01]
KAUST Base Research Funds [BAS/1/1606-01-01] KAUST grant OSR#4 129
KAUST Office of Sponsored Research (OSR) [FCC/1/1976-17-01] KAUST Office of Sponsored Research (OSR) [FCC/1/1976‐17‐01]
KAUST Office of Sponsored Research (OSR) [FCC/1/1976‐24‐01] KAUST [OSR#4129]
Ministry of Science and Technological Development of the Republic of Serbia [145073, 145058] Ministry of Science of the Republic of Serbia [145073, 145067, 143030]
Ministry of Science, Republic of Serbia [143030] Ministry of Science, Republic of Serbia [143030B, 145073]
Novo Nordisk Foundation, European Commission [COST BM0602]

Author's Bibliography

Effect of Hyperbaric Oxygen Therapy on Fatty Acid Composition and Insulin-like Growth Factor Binding Protein 1 in Adult Type 1 Diabetes Mellitus Patients: A Pilot Study

Resanović, Ivana; Gluvić, Zoran; Zarić, Božidarka; Sudar-Milovanović, Emina; Vučić, Vesna; Arsić, Aleksandra; Nedić, Olgica; Šunderić, Miloš; Gligorijević, Nikola; Milačić, Davorka; Isenović, Esma R.

(2020)

TY  - JOUR
AU  - Resanović, Ivana
AU  - Gluvić, Zoran
AU  - Zarić, Božidarka
AU  - Sudar-Milovanović, Emina
AU  - Vučić, Vesna
AU  - Arsić, Aleksandra
AU  - Nedić, Olgica
AU  - Šunderić, Miloš
AU  - Gligorijević, Nikola
AU  - Milačić, Davorka
AU  - Isenović, Esma R.
PY  - 2020
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8567
AB  - Objective: Metabolic changes in insulin-dependent diabetes mellitus (IDDM) impair vasodilation, and this leads to tissue hypoxia and microvascular pathology. Hyperbaric oxygen therapy (HBOT) can significantly improve the outcome of ischemic conditions in IDDM patients and reduce vascular complications. The aim of our study was to assess the effects of HBOT on plasma fatty acid (FA) composition, and expression of insulin-like growth factor binding protein 1 (IGFBP-1) in IDDM patients. Methods: Our study included 24 adult IDDM patients diagnosed with peripheral vascular complications. The patients were exposed to 10 sessions of 100% oxygen inhalation at 2.4 atmosphere absolute for 1 hour. Blood samples were collected at admission and after HBOT for measurement of metabolic parameters, FA composition and IGFBP-1. Measurement of plasma FA composition was determined by gas chromatography. Expression of IGFBP-1 in the serum was estimated by Western blot analysis. Results: HBOT decreased blood levels of total cholesterol (p<0.05), triglycerides (p<0.05) and low-density lipoprotein (p<0.05). HBOT increased plasma levels of individual FAs: palmitic acid (p<0.05), palmitoleic acid (p<0.05), docosapentaenoic acid (p<0.05) and docosahexaenoic acid (p<0.01), and decreased levels of stearic acid (p<0.05), alpha linolenic acid (p<0.05) and linoleic acid (p<0.01). Expression of IGFBP-1 (p<0.01) was increased, whereas the level of insulin (p<0.001) was decreased in the serum after HBOT. Conclusions: Our results indicate that HBOT exerts beneficial effects in IDDM patients by improving the lipid profile and altering FA composition. © 2019 Canadian Diabetes Association
T2  - Canadian Journal of Diabetes
T1  - Effect of Hyperbaric Oxygen Therapy on Fatty Acid Composition and Insulin-like Growth Factor Binding Protein 1 in Adult Type 1 Diabetes Mellitus Patients: A Pilot Study
VL  - 44
IS  - 1
SP  - 22
EP  - 29
DO  - 10.1016/j.jcjd.2019.04.018
ER  - 
@article{
author = "Resanović, Ivana and Gluvić, Zoran and Zarić, Božidarka and Sudar-Milovanović, Emina and Vučić, Vesna and Arsić, Aleksandra and Nedić, Olgica and Šunderić, Miloš and Gligorijević, Nikola and Milačić, Davorka and Isenović, Esma R.",
year = "2020",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8567",
abstract = "Objective: Metabolic changes in insulin-dependent diabetes mellitus (IDDM) impair vasodilation, and this leads to tissue hypoxia and microvascular pathology. Hyperbaric oxygen therapy (HBOT) can significantly improve the outcome of ischemic conditions in IDDM patients and reduce vascular complications. The aim of our study was to assess the effects of HBOT on plasma fatty acid (FA) composition, and expression of insulin-like growth factor binding protein 1 (IGFBP-1) in IDDM patients. Methods: Our study included 24 adult IDDM patients diagnosed with peripheral vascular complications. The patients were exposed to 10 sessions of 100% oxygen inhalation at 2.4 atmosphere absolute for 1 hour. Blood samples were collected at admission and after HBOT for measurement of metabolic parameters, FA composition and IGFBP-1. Measurement of plasma FA composition was determined by gas chromatography. Expression of IGFBP-1 in the serum was estimated by Western blot analysis. Results: HBOT decreased blood levels of total cholesterol (p<0.05), triglycerides (p<0.05) and low-density lipoprotein (p<0.05). HBOT increased plasma levels of individual FAs: palmitic acid (p<0.05), palmitoleic acid (p<0.05), docosapentaenoic acid (p<0.05) and docosahexaenoic acid (p<0.01), and decreased levels of stearic acid (p<0.05), alpha linolenic acid (p<0.05) and linoleic acid (p<0.01). Expression of IGFBP-1 (p<0.01) was increased, whereas the level of insulin (p<0.001) was decreased in the serum after HBOT. Conclusions: Our results indicate that HBOT exerts beneficial effects in IDDM patients by improving the lipid profile and altering FA composition. © 2019 Canadian Diabetes Association",
journal = "Canadian Journal of Diabetes",
title = "Effect of Hyperbaric Oxygen Therapy on Fatty Acid Composition and Insulin-like Growth Factor Binding Protein 1 in Adult Type 1 Diabetes Mellitus Patients: A Pilot Study",
volume = "44",
number = "1",
pages = "22-29",
doi = "10.1016/j.jcjd.2019.04.018"
}
1
1
1
1

Regulation of nitric oxide production in hypothyroidism

Gluvić, Zoran; Obradović, Milan M.; Sudar-Milovanović, Emina; Zafirović, Sonja; Radak, Đorđe J.; Essack, Magbubah; Bajić, Vladimir B.; Gojobori, Takashi; Isenović, Esma R.

(2020)

TY  - JOUR
AU  - Gluvić, Zoran
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Zafirović, Sonja
AU  - Radak, Đorđe J.
AU  - Essack, Magbubah
AU  - Bajić, Vladimir B.
AU  - Gojobori, Takashi
AU  - Isenović, Esma R.
PY  - 2020
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8474
AB  - Hypothyroidism is a common endocrine disorder that predominantly occurs in females. It is associated with an increased risk of cardiovascular diseases (CVD), but the molecular mechanism is not known. Disturbance in lipid metabolism, the regulation of oxidative stress, and inflammation characterize the progression of subclinical hypothyroidism. The initiation and progression of endothelial dysfunction also exhibit these changes, which is the initial step in developing CVD. Animal and human studies highlight the critical role of nitric oxide (NO) as a reliable biomarker for cardiovascular risk in subclinical and clinical hypothyroidism. In this review, we summarize the recent literature findings associated with NO production by the thyroid hormones in both physiological and pathophysiological conditions. We also discuss the levothyroxine treatment effect on serum NO levels in hypothyroid patients. © 2020 The Authors
T2  - Biomedicine & Pharmacotherapy
T1  - Regulation of nitric oxide production in hypothyroidism
VL  - 124
SP  - 109881
DO  - 10.1016/j.biopha.2020.109881
ER  - 
@article{
author = "Gluvić, Zoran and Obradović, Milan M. and Sudar-Milovanović, Emina and Zafirović, Sonja and Radak, Đorđe J. and Essack, Magbubah and Bajić, Vladimir B. and Gojobori, Takashi and Isenović, Esma R.",
year = "2020",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8474",
abstract = "Hypothyroidism is a common endocrine disorder that predominantly occurs in females. It is associated with an increased risk of cardiovascular diseases (CVD), but the molecular mechanism is not known. Disturbance in lipid metabolism, the regulation of oxidative stress, and inflammation characterize the progression of subclinical hypothyroidism. The initiation and progression of endothelial dysfunction also exhibit these changes, which is the initial step in developing CVD. Animal and human studies highlight the critical role of nitric oxide (NO) as a reliable biomarker for cardiovascular risk in subclinical and clinical hypothyroidism. In this review, we summarize the recent literature findings associated with NO production by the thyroid hormones in both physiological and pathophysiological conditions. We also discuss the levothyroxine treatment effect on serum NO levels in hypothyroid patients. © 2020 The Authors",
journal = "Biomedicine & Pharmacotherapy",
title = "Regulation of nitric oxide production in hypothyroidism",
volume = "124",
pages = "109881",
doi = "10.1016/j.biopha.2020.109881"
}
1

Redox control of vascular biology

Obradović, Milan M.; Essack, Magbubah; Zafirović, Sonja; Sudar-Milovanović, Emina; Bajić, Vladan P.; Van Neste, Christophe; Trpković, Andreja; Stanimirović, Julijana; Bajić, Vladimir B.; Isenović, Esma R.

(2020)

@article{
author = "Obradović, Milan M. and Essack, Magbubah and Zafirović, Sonja and Sudar-Milovanović, Emina and Bajić, Vladan P. and Van Neste, Christophe and Trpković, Andreja and Stanimirović, Julijana and Bajić, Vladimir B. and Isenović, Esma R.",
year = "2020",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8486",
abstract = "Redox control is lost when the antioxidant defense system cannot remove abnormally high concentrations of signaling molecules, such as reactive oxygen species (ROS). Chronically elevated levels of ROS cause oxidative stress that may eventually lead to cancer and cardiovascular and neurodegenerative diseases. In this review, we focus on redox effects in the vascular system. We pay close attention to the subcompartments of the vascular system (endothelium, smooth muscle cell layer) and give an overview of how redox changes influence those different compartments. We also review the core aspects of redox biology, cardiovascular physiology, and pathophysiology. Moreover, the topic-specific knowledgebase DES-RedoxVasc was used to develop two case studies, one focused on endothelial cells and the other on the vascular smooth muscle cells, as a starting point to possibly extend our knowledge of redox control in vascular biology. © 2019 The Authors. BioFactors published by Wiley Periodicals, Inc. on behalf of International Union of Biochemistry and Molecular Biology.",
journal = "BioFactors",
title = "Redox control of vascular biology",
volume = "46",
number = "2",
pages = "246-262",
doi = "10.1002/biof.1559"
}
3
3
1

Drug Delivery Systems for Diabetes Treatment

Zarić, Božidarka; Obradović, Milan M.; Sudar-Milovanović, Emina; Nedeljković, Jovan; Lazić, Vesna M.; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Zarić, Božidarka
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Nedeljković, Jovan
AU  - Lazić, Vesna M.
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8378
AB  - Background: Insulin is essential for the treatment of Type 1 diabetes mellitus (T1DM) and is necessary in numerous cases of Type 2 diabetes mellitus (T2DM). Prolonged administration of anti-diabetic therapy is necessary for the maintenance of the normal glucose levels and thereby preventing vascular complications. A better understanding of the disease per se and the technological progress contribute to the development of new approaches with the aim to achieve better glycemic control. Objective: Current therapies for DM are faced with some challenges. The purpose of this review is to analyze in detail the current trends for insulin delivery systems for diabetes treatment. Results: Contemporary ways have been proposed for the management of both types of diabetes by adequate application of drug via subcutaneous, buccal, oral, ocular, nasal, rectal and pulmonary ways. Development of improved oral administration of insulin is beneficial regarding mimicking physiological pathway of insulin and minimizing the discomfort of the patient. Various nanoparticle carriers for oral and other ways of insulin delivery are currently being developed. Engineered specific properties of nanoparticles (NP): controlling toxicity of NP, stability and drug release, can allow delivery of higher concentration of the drug to the desired location. Conclusions: The successful development of any drug delivery system relies on solving three important issues: toxicity of nanoparticles, stability of nanoparticles, and desired drug release rate at targeted sites. The main goals of future investigations are to improve the existing therapies by pharmacokinetic modifications, development of a fully automatized system to mimic insulin delivery by the pancreas and reduce invasiveness during admission. © 2019 Bentham Science Publishers.
T2  - Current Pharmaceutical Design
T1  - Drug Delivery Systems for Diabetes Treatment
VL  - 25
IS  - 2
SP  - 166
EP  - 173
DO  - 10.2174/1381612825666190306153838
ER  - 
@article{
author = "Zarić, Božidarka and Obradović, Milan M. and Sudar-Milovanović, Emina and Nedeljković, Jovan and Lazić, Vesna M. and Isenović, Esma R.",
year = "2019",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8378",
abstract = "Background: Insulin is essential for the treatment of Type 1 diabetes mellitus (T1DM) and is necessary in numerous cases of Type 2 diabetes mellitus (T2DM). Prolonged administration of anti-diabetic therapy is necessary for the maintenance of the normal glucose levels and thereby preventing vascular complications. A better understanding of the disease per se and the technological progress contribute to the development of new approaches with the aim to achieve better glycemic control. Objective: Current therapies for DM are faced with some challenges. The purpose of this review is to analyze in detail the current trends for insulin delivery systems for diabetes treatment. Results: Contemporary ways have been proposed for the management of both types of diabetes by adequate application of drug via subcutaneous, buccal, oral, ocular, nasal, rectal and pulmonary ways. Development of improved oral administration of insulin is beneficial regarding mimicking physiological pathway of insulin and minimizing the discomfort of the patient. Various nanoparticle carriers for oral and other ways of insulin delivery are currently being developed. Engineered specific properties of nanoparticles (NP): controlling toxicity of NP, stability and drug release, can allow delivery of higher concentration of the drug to the desired location. Conclusions: The successful development of any drug delivery system relies on solving three important issues: toxicity of nanoparticles, stability of nanoparticles, and desired drug release rate at targeted sites. The main goals of future investigations are to improve the existing therapies by pharmacokinetic modifications, development of a fully automatized system to mimic insulin delivery by the pancreas and reduce invasiveness during admission. © 2019 Bentham Science Publishers.",
journal = "Current Pharmaceutical Design",
title = "Drug Delivery Systems for Diabetes Treatment",
volume = "25",
number = "2",
pages = "166-173",
doi = "10.2174/1381612825666190306153838"
}
4
3
4

Involvement of PI3K, Akt and RhoA in Oestradiol Regulation of Cardiac iNOS Expression

Zafirović, Sonja; Sudar-Milovanović, Emina; Obradović, Milan M.; Đorđević, Jelena D.; Jasnić, Nebojša; Labudović-Borović, Milica; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Zafirović, Sonja
AU  - Sudar-Milovanović, Emina
AU  - Obradović, Milan M.
AU  - Đorđević, Jelena D.
AU  - Jasnić, Nebojša
AU  - Labudović-Borović, Milica
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://www.eurekaselect.com/159734/article
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8097
AB  - BACKGROUND: Oestradiol is an important regulatory factor with several positive effects on the cardiovascular (CV) system. We evaluated the molecular mechanism of the in vivo effects of oestradiol on the regulation of cardiac inducible nitric oxide (NO) synthase (iNOS) expression and activity. METHODS: Male Wistar rats were treated with oestradiol (40 mg/kg, intraperitoneally) and after 24 h the animals were sacrificed. The concentrations of NO and L-Arginine (L-Arg) were determined spectrophotometrically. For protein expressions of iNOS, p65 subunit of nuclear factor-κB (NFκB-p65), Ras homolog gene family-member A (RhoA), angiotensin II receptor type 1 (AT1R), insulin receptor substrate 1 (IRS-1), p85, p110 and protein kinase B (Akt), Western blot method was used. Coimmunoprecipitation was used for measuring the association of IRS-1 with the p85 subunit of phosphatidylinositol- 3-kinase (PI3K). The expression of iNOS messenger ribonucleic acid (mRNA) was measured with the quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemical analysis of the tissue was used to detect localization and expression of iNOS in heart tissue. RESULTS: Oestradiol treatment reduced L-Arg concentration (p<0.01), iNOS mRNA (p<0.01) and protein (p<0.001) expression, level of RhoA (p<0.05) and AT1R (p<0.001) protein. In contrast, plasma NO (p<0.05), Akt phosphorylation at Thr308 (p<0.05) and protein level of p85 (p<0.001) increased after oestradiol treatment. CONCLUSION: Our results suggest that oestradiol in vivo regulates cardiac iNOS expression via the PI3K/Akt signaling pathway, through attenuation of RhoA and AT1R.
T2  - Current Vascular Pharmacology
T1  - Involvement of PI3K, Akt and RhoA in Oestradiol Regulation of Cardiac iNOS Expression
VL  - 17
IS  - 3
SP  - 307
EP  - 318
DO  - 10.2174/1570161116666180212142414
ER  - 
@article{
author = "Zafirović, Sonja and Sudar-Milovanović, Emina and Obradović, Milan M. and Đorđević, Jelena D. and Jasnić, Nebojša and Labudović-Borović, Milica and Isenović, Esma R.",
year = "2019",
url = "http://www.eurekaselect.com/159734/article, http://vinar.vin.bg.ac.rs/handle/123456789/8097",
abstract = "BACKGROUND: Oestradiol is an important regulatory factor with several positive effects on the cardiovascular (CV) system. We evaluated the molecular mechanism of the in vivo effects of oestradiol on the regulation of cardiac inducible nitric oxide (NO) synthase (iNOS) expression and activity. METHODS: Male Wistar rats were treated with oestradiol (40 mg/kg, intraperitoneally) and after 24 h the animals were sacrificed. The concentrations of NO and L-Arginine (L-Arg) were determined spectrophotometrically. For protein expressions of iNOS, p65 subunit of nuclear factor-κB (NFκB-p65), Ras homolog gene family-member A (RhoA), angiotensin II receptor type 1 (AT1R), insulin receptor substrate 1 (IRS-1), p85, p110 and protein kinase B (Akt), Western blot method was used. Coimmunoprecipitation was used for measuring the association of IRS-1 with the p85 subunit of phosphatidylinositol- 3-kinase (PI3K). The expression of iNOS messenger ribonucleic acid (mRNA) was measured with the quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemical analysis of the tissue was used to detect localization and expression of iNOS in heart tissue. RESULTS: Oestradiol treatment reduced L-Arg concentration (p<0.01), iNOS mRNA (p<0.01) and protein (p<0.001) expression, level of RhoA (p<0.05) and AT1R (p<0.001) protein. In contrast, plasma NO (p<0.05), Akt phosphorylation at Thr308 (p<0.05) and protein level of p85 (p<0.001) increased after oestradiol treatment. CONCLUSION: Our results suggest that oestradiol in vivo regulates cardiac iNOS expression via the PI3K/Akt signaling pathway, through attenuation of RhoA and AT1R.",
journal = "Current Vascular Pharmacology",
title = "Involvement of PI3K, Akt and RhoA in Oestradiol Regulation of Cardiac iNOS Expression",
volume = "17",
number = "3",
pages = "307-318",
doi = "10.2174/1570161116666180212142414"
}
1
1
1

Hypothesis regarding the effects of gonadotropins on the level of free fatty acids and phospholipids in serum and follicular fluid during controlled ovarian stimulation

Perović, Milan; Sudar-Milovanović, Emina; Simonović, Ema D.; Resanović, Ivana; Draganić, Veselin D.; Radaković, Jovana D.; Soldatović, Ivan A.; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Perović, Milan
AU  - Sudar-Milovanović, Emina
AU  - Simonović, Ema D.
AU  - Resanović, Ivana
AU  - Draganić, Veselin D.
AU  - Radaković, Jovana D.
AU  - Soldatović, Ivan A.
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0306987718310892
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8006
AB  - Controlled ovarian stimulation (COS) is used to augment the number of retrieved oocytes in in vitro fertilization (IVF). Follicular fluid (FF) contributes significantly to oocyte quality. Since the FF is composed of follicular secretions and plasma exudation, it reflects alterations in granulosa and thecal cells secretion as well as changes in the level of plasma constituents. Phospholipids (PL) and free fatty acids (FFA) are important constituents of both, FF and serum. Our hypothesis is that COS affects the level of PL and FFA in serum. Furthermore, since the level of PL and FFA in FF partially depends on their levels in serum, as a collaterally of our hypothesis is that the existing level of PL and FFA in serum correlates with the levels of PL and FFA in FF, and that the dose of applied gonadotropins during COS will correlate with the levels of PL and FFA in serum and FF. In addition, we assume that the level of PL and FFA in serum and in FF after COS will correlate with the retrieved number of GQ oocytes, one of the most important outcomes of COS.. © 2018
T2  - Medical Hypotheses
T1  - Hypothesis regarding the effects of gonadotropins on the level of free fatty acids and phospholipids in serum and follicular fluid during controlled ovarian stimulation
VL  - 123
SP  - 30
EP  - 34
DO  - 10.1016/j.mehy.2018.11.021
ER  - 
@article{
author = "Perović, Milan and Sudar-Milovanović, Emina and Simonović, Ema D. and Resanović, Ivana and Draganić, Veselin D. and Radaković, Jovana D. and Soldatović, Ivan A. and Isenović, Esma R.",
year = "2019",
url = "https://linkinghub.elsevier.com/retrieve/pii/S0306987718310892, http://vinar.vin.bg.ac.rs/handle/123456789/8006",
abstract = "Controlled ovarian stimulation (COS) is used to augment the number of retrieved oocytes in in vitro fertilization (IVF). Follicular fluid (FF) contributes significantly to oocyte quality. Since the FF is composed of follicular secretions and plasma exudation, it reflects alterations in granulosa and thecal cells secretion as well as changes in the level of plasma constituents. Phospholipids (PL) and free fatty acids (FFA) are important constituents of both, FF and serum. Our hypothesis is that COS affects the level of PL and FFA in serum. Furthermore, since the level of PL and FFA in FF partially depends on their levels in serum, as a collaterally of our hypothesis is that the existing level of PL and FFA in serum correlates with the levels of PL and FFA in FF, and that the dose of applied gonadotropins during COS will correlate with the levels of PL and FFA in serum and FF. In addition, we assume that the level of PL and FFA in serum and in FF after COS will correlate with the retrieved number of GQ oocytes, one of the most important outcomes of COS.. © 2018",
journal = "Medical Hypotheses",
title = "Hypothesis regarding the effects of gonadotropins on the level of free fatty acids and phospholipids in serum and follicular fluid during controlled ovarian stimulation",
volume = "123",
pages = "30-34",
doi = "10.1016/j.mehy.2018.11.021"
}
4
4
4

Serum nitric oxide levels correlate with quality of life questionnaires scores of hypothyroid females

Gluvić, Zoran; Sudar-Milovanović, Emina; Samardžić, Vladimir S.; Obradović, Milan M.; Jevremović, Danimir P.; Radenković, Saša P.; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Gluvić, Zoran
AU  - Sudar-Milovanović, Emina
AU  - Samardžić, Vladimir S.
AU  - Obradović, Milan M.
AU  - Jevremović, Danimir P.
AU  - Radenković, Saša P.
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8369
AB  - Primary hypothyroidism can affect lipid metabolism, cardiovascular (CV) function, and overall patients’ quality of life (QoL). Decrease in serum nitric oxide (NO) levels could promote the atherosclerosis acceleration in hypothyroid patients. Our hypothesis is that serum NO level is altered in hypothyroidism; more specifically, we hypothesize that the early vascular changes that can be observed in hypothyroidism could be due to these alterations and that serum NO levels are associated with lipid levels in female patients diagnosed with subclinical hypothyroidism (SCH) or clinical hypothyroidism (CH). Furthermore, since serum NO level is an early marker of atherosclerosis and related CV disorders, which are commonly present and follow hypothyreosis and greatly contribute to overall QoL, we further hypothesized that NO level would correlate with Thyroid Symptom Questionnaire (TSQ) and General Health Questionnaire 12 (GHQ12) scores in hypothyroid patients. A collaterally of our hypothesis was that levothyroxine (LT4) treatment would affect serum NO levels as well as TSQ and GHQ12 scores. Therefore, we have analyzed lipid profile, the level of NO and QoL scores in female patients diagnosed with SCH and CH in order to determine the correlation between NO and generic and thyroid disease symptoms in treatment naïve SCH and CH patients and after LT4 treatment and laboratory euthyroidism achievement. As a consequence of our hypothesis is that measurement of serum NO level in SCH and CH patients may be an innovative way to improve LT4 treatment efficacy. This assumption could have a practical significance for future investigations regarding the management of hypothyroidism treatment protocols in current guidelines. © 2019 Elsevier Ltd
T2  - Medical Hypotheses
T1  - Serum nitric oxide levels correlate with quality of life questionnaires scores of hypothyroid females
VL  - 131
SP  - 109299
DO  - 10.1016/j.mehy.2019.109299
ER  - 
@article{
author = "Gluvić, Zoran and Sudar-Milovanović, Emina and Samardžić, Vladimir S. and Obradović, Milan M. and Jevremović, Danimir P. and Radenković, Saša P. and Isenović, Esma R.",
year = "2019",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8369",
abstract = "Primary hypothyroidism can affect lipid metabolism, cardiovascular (CV) function, and overall patients’ quality of life (QoL). Decrease in serum nitric oxide (NO) levels could promote the atherosclerosis acceleration in hypothyroid patients. Our hypothesis is that serum NO level is altered in hypothyroidism; more specifically, we hypothesize that the early vascular changes that can be observed in hypothyroidism could be due to these alterations and that serum NO levels are associated with lipid levels in female patients diagnosed with subclinical hypothyroidism (SCH) or clinical hypothyroidism (CH). Furthermore, since serum NO level is an early marker of atherosclerosis and related CV disorders, which are commonly present and follow hypothyreosis and greatly contribute to overall QoL, we further hypothesized that NO level would correlate with Thyroid Symptom Questionnaire (TSQ) and General Health Questionnaire 12 (GHQ12) scores in hypothyroid patients. A collaterally of our hypothesis was that levothyroxine (LT4) treatment would affect serum NO levels as well as TSQ and GHQ12 scores. Therefore, we have analyzed lipid profile, the level of NO and QoL scores in female patients diagnosed with SCH and CH in order to determine the correlation between NO and generic and thyroid disease symptoms in treatment naïve SCH and CH patients and after LT4 treatment and laboratory euthyroidism achievement. As a consequence of our hypothesis is that measurement of serum NO level in SCH and CH patients may be an innovative way to improve LT4 treatment efficacy. This assumption could have a practical significance for future investigations regarding the management of hypothyroidism treatment protocols in current guidelines. © 2019 Elsevier Ltd",
journal = "Medical Hypotheses",
title = "Serum nitric oxide levels correlate with quality of life questionnaires scores of hypothyroid females",
volume = "131",
pages = "109299",
doi = "10.1016/j.mehy.2019.109299"
}
1
1
2

Early Effects of Hyperbaric Oxygen on Inducible Nitric Oxide Synthase Activity/Expression in Lymphocytes of Type 1 Diabetes Patients: A Prospective Pilot Study

Resanović, Ivana; Gluvić, Zoran; Zarić, Božidarka; Sudar-Milovanović, Emina; Jovanović, Aleksandra; Milačić, Davorka; Isaković, Radmilo; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Resanović, Ivana
AU  - Gluvić, Zoran
AU  - Zarić, Božidarka
AU  - Sudar-Milovanović, Emina
AU  - Jovanović, Aleksandra
AU  - Milačić, Davorka
AU  - Isaković, Radmilo
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://www.hindawi.com/journals/ije/2019/2328505/
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8209
AB  - This study aimed at examining the early effects of hyperbaric oxygen therapy (HBOT) on inducible nitric oxide synthase (iNOS) activity/expression in lymphocytes of type 1 diabetes mellitus (T1DM) patients. A group of 19 patients (mean age: 63 ± 2.1) with T1DM and with the peripheral arterial disease were included in this study. Patients were exposed to 10 sessions of HBOT in the duration of 1 h to 100% oxygen inhalation at 2.4 ATA. Blood samples were collected for the plasma C-reactive protein (CRP), plasma free fatty acid (FFA), serum nitrite/nitrate, and serum arginase activity measurements. Expression of iNOS and phosphorylation of p65 subunit of nuclear factor- κ B (NF κ B-p65), extracellular-regulated kinases 1/2 (ERK1/2), and protein kinase B (Akt) were examined in lymphocyte lysates by Western blot. After exposure to HBOT, plasma CRP and FFA were significantly decreased ( p < 0.001 ). Protein expression of iNOS and serum nitrite/nitrate levels were decreased ( p < 0.01 ), while serum arginase activity was increased ( p < 0.05 ) versus before exposure to HBOT. Increased phosphorylation of NF κ B-p65 at Ser 536 ( p < 0.05 ) and decreased level of NF κ B-p65 protein ( p < 0.001 ) in lymphocytes of T1DM patients were observed after HBOT. Decreased phosphorylation of ERK1/2 ( p < 0.05 ) and Akt ( p < 0.05 ) was detected after HBOT. Our results indicate that exposure to HBO decreased iNOS activity/expression via decreasing phosphorylation of ERK1/2 and Akt followed by decreased activity of NF κ B.
T2  - International Journal of Endocrinology
T1  - Early Effects of Hyperbaric Oxygen on Inducible Nitric Oxide Synthase Activity/Expression in Lymphocytes of Type 1 Diabetes Patients: A Prospective Pilot Study
VL  - 2019
SP  - 1
EP  - 12
DO  - 10.1155/2019/2328505
ER  - 
@article{
author = "Resanović, Ivana and Gluvić, Zoran and Zarić, Božidarka and Sudar-Milovanović, Emina and Jovanović, Aleksandra and Milačić, Davorka and Isaković, Radmilo and Isenović, Esma R.",
year = "2019",
url = "https://www.hindawi.com/journals/ije/2019/2328505/, http://vinar.vin.bg.ac.rs/handle/123456789/8209",
abstract = "This study aimed at examining the early effects of hyperbaric oxygen therapy (HBOT) on inducible nitric oxide synthase (iNOS) activity/expression in lymphocytes of type 1 diabetes mellitus (T1DM) patients. A group of 19 patients (mean age: 63 ± 2.1) with T1DM and with the peripheral arterial disease were included in this study. Patients were exposed to 10 sessions of HBOT in the duration of 1 h to 100% oxygen inhalation at 2.4 ATA. Blood samples were collected for the plasma C-reactive protein (CRP), plasma free fatty acid (FFA), serum nitrite/nitrate, and serum arginase activity measurements. Expression of iNOS and phosphorylation of p65 subunit of nuclear factor- κ B (NF κ B-p65), extracellular-regulated kinases 1/2 (ERK1/2), and protein kinase B (Akt) were examined in lymphocyte lysates by Western blot. After exposure to HBOT, plasma CRP and FFA were significantly decreased ( p < 0.001 ). Protein expression of iNOS and serum nitrite/nitrate levels were decreased ( p < 0.01 ), while serum arginase activity was increased ( p < 0.05 ) versus before exposure to HBOT. Increased phosphorylation of NF κ B-p65 at Ser 536 ( p < 0.05 ) and decreased level of NF κ B-p65 protein ( p < 0.001 ) in lymphocytes of T1DM patients were observed after HBOT. Decreased phosphorylation of ERK1/2 ( p < 0.05 ) and Akt ( p < 0.05 ) was detected after HBOT. Our results indicate that exposure to HBO decreased iNOS activity/expression via decreasing phosphorylation of ERK1/2 and Akt followed by decreased activity of NF κ B.",
journal = "International Journal of Endocrinology",
title = "Early Effects of Hyperbaric Oxygen on Inducible Nitric Oxide Synthase Activity/Expression in Lymphocytes of Type 1 Diabetes Patients: A Prospective Pilot Study",
volume = "2019",
pages = "1-12",
doi = "10.1155/2019/2328505"
}
3
2
1

Genetic Markers for Coronary Artery Disease

Veljković, Nevena V.; Zarić, Božidarka; Đurić, Ilona; Obradović, Milan M.; Sudar-Milovanović, Emina; Radak, Đorđe J.; Isenović, Esma R.

(2018)

TY  - JOUR
AU  - Veljković, Nevena V.
AU  - Zarić, Božidarka
AU  - Đurić, Ilona
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2018
UR  - http://www.mdpi.com/1010-660X/54/3/36
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7878
AB  - Coronary artery disease (CAD) and myocardial infarction (MI) are recognized as leading causes of mortality in developed countries. Although typically associated with behavioral risk factors, such as smoking, sedentary lifestyle, and poor dietary habits, such vascular phenotypes have also long been recognized as being related to genetic background. We review the currently available data concerning genetic markers for CAD in English and non-English articles with English abstracts published between 2003 and 2018. As genetic testing is increasingly available, it may be possible to identify adequate genetic markers representing the risk profile and to use them in a clinical setting. © 2018 by the authors. Licensee MDPI, Basel, Switzerland.
T2  - Medicina
T1  - Genetic Markers for Coronary Artery Disease
VL  - 54
IS  - 3
SP  - 36
DO  - 10.3390/medicina54030036
ER  - 
@article{
author = "Veljković, Nevena V. and Zarić, Božidarka and Đurić, Ilona and Obradović, Milan M. and Sudar-Milovanović, Emina and Radak, Đorđe J. and Isenović, Esma R.",
year = "2018",
url = "http://www.mdpi.com/1010-660X/54/3/36, http://vinar.vin.bg.ac.rs/handle/123456789/7878",
abstract = "Coronary artery disease (CAD) and myocardial infarction (MI) are recognized as leading causes of mortality in developed countries. Although typically associated with behavioral risk factors, such as smoking, sedentary lifestyle, and poor dietary habits, such vascular phenotypes have also long been recognized as being related to genetic background. We review the currently available data concerning genetic markers for CAD in English and non-English articles with English abstracts published between 2003 and 2018. As genetic testing is increasingly available, it may be possible to identify adequate genetic markers representing the risk profile and to use them in a clinical setting. © 2018 by the authors. Licensee MDPI, Basel, Switzerland.",
journal = "Medicina",
title = "Genetic Markers for Coronary Artery Disease",
volume = "54",
number = "3",
pages = "36",
doi = "10.3390/medicina54030036"
}
1
2
2
3

Estradiol‐mediated regulation of hepatic iNOS in obese rats: Impact of Src, ERK1/2, AMPKα, and miR‐221

Panić, Anastasija; Stanimirović, Julijana; Obradović, Milan M.; Sudar-Milovanović, Emina; Perović, Milan; Lačković, Milena; Petrović, Nina; Isenović, Esma R.

(2018)

TY  - JOUR
AU  - Panić, Anastasija
AU  - Stanimirović, Julijana
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Perović, Milan
AU  - Lačković, Milena
AU  - Petrović, Nina
AU  - Isenović, Esma R.
PY  - 2018
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8399
AB  - Purpose: This study aimed to investigate in vivo effects of estradiol on the regulation of hepatic inducible nitric oxide synthase (iNOS) expression in the high fat (HF) diet-induced obesity. Also, we aimed to investigate whether activation of the extracellular signal-regulated kinase (ERK1/2), adenosine monophosphate-activated protein kinase (AMPK), Src kinase, and miR-221 is involved in estradiol-mediated regulation of iNOS in the liver of obese male Wistar rats. Male Wistar rats were fed a standard laboratory diet or a HF diet for 10 weeks. Half of HF rats were treated with estradiol intraperitoneally (40 μg/kg), whereas the other half were placebo-treated 24 H before euthanasia. Results show that estradiol treatment of HF rats decreased hepatic iNOS mRNA (P < 0.05) and protein expression (P < 0.01), the protein levels of p65 subunit of nuclear factor κB (P < 0.05) and ERα (P < 0.05), ERK1/2 phosphorylation (P < 0.001), and ERα/Src kinase association (P < 0.05). By contrast, hepatic Src protein level (P < 0.05), AMPKα phosphorylation (P < 0.05), and miR-221 expression (P < 0.05) were increased in HF rats after estradiol treatment. Our results indicate that estradiol in vivo regulates hepatic iNOS expression in obese rats via molecular mechanisms involving ERK1/2, AMPK, Src, and miR-221 signaling. © 2018 International Union of Biochemistry and Molecular Biology, Inc.
T2  - Biotechnology and Applied Biochemistry
T1  - Estradiol‐mediated regulation of hepatic iNOS in obese rats: Impact of Src, ERK1/2, AMPKα, and miR‐221
VL  - 65
IS  - 6
SP  - 797
EP  - 806
DO  - 10.1002/bab.1680
ER  - 
@article{
author = "Panić, Anastasija and Stanimirović, Julijana and Obradović, Milan M. and Sudar-Milovanović, Emina and Perović, Milan and Lačković, Milena and Petrović, Nina and Isenović, Esma R.",
year = "2018",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8399",
abstract = "Purpose: This study aimed to investigate in vivo effects of estradiol on the regulation of hepatic inducible nitric oxide synthase (iNOS) expression in the high fat (HF) diet-induced obesity. Also, we aimed to investigate whether activation of the extracellular signal-regulated kinase (ERK1/2), adenosine monophosphate-activated protein kinase (AMPK), Src kinase, and miR-221 is involved in estradiol-mediated regulation of iNOS in the liver of obese male Wistar rats. Male Wistar rats were fed a standard laboratory diet or a HF diet for 10 weeks. Half of HF rats were treated with estradiol intraperitoneally (40 μg/kg), whereas the other half were placebo-treated 24 H before euthanasia. Results show that estradiol treatment of HF rats decreased hepatic iNOS mRNA (P < 0.05) and protein expression (P < 0.01), the protein levels of p65 subunit of nuclear factor κB (P < 0.05) and ERα (P < 0.05), ERK1/2 phosphorylation (P < 0.001), and ERα/Src kinase association (P < 0.05). By contrast, hepatic Src protein level (P < 0.05), AMPKα phosphorylation (P < 0.05), and miR-221 expression (P < 0.05) were increased in HF rats after estradiol treatment. Our results indicate that estradiol in vivo regulates hepatic iNOS expression in obese rats via molecular mechanisms involving ERK1/2, AMPK, Src, and miR-221 signaling. © 2018 International Union of Biochemistry and Molecular Biology, Inc.",
journal = "Biotechnology and Applied Biochemistry",
title = "Estradiol‐mediated regulation of hepatic iNOS in obese rats: Impact of Src, ERK1/2, AMPKα, and miR‐221",
volume = "65",
number = "6",
pages = "797-806",
doi = "10.1002/bab.1680"
}
3
2
2

The role of eNOS and iNOS in pathophysiological conditions

Obradović, Milan M.; Zarić, Božidarka; Sudar-Milovanović, Emina; Perović, Milan; Resanović, Ivana; Gluvić, Zoran; Isenović, Esma R.

(Nova Science Publishers, 2018)

TY  - CHAP
AU  - Obradović, Milan M.
AU  - Zarić, Božidarka
AU  - Sudar-Milovanović, Emina
AU  - Perović, Milan
AU  - Resanović, Ivana
AU  - Gluvić, Zoran
AU  - Isenović, Esma R.
PY  - 2018
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8014
AB  - Nitric oxide (NO) is a free radical which, in reactions with various molecules causes multiple biological effects. NO is exceptionally regulated and extends to almost every cell type and function within circulation. Generation and actions of NO are regulated by various hormones under physiological and pathophysiological conditions. Nitric oxide synthases (NOS) are the enzymes responsible for NO generation. In mammals, neuronal NOS (nNOS) and endothelial NOS (eNOS) are constitutively expressed, while inducible NOS (iNOS) mediate in immune defense. Altered NO level is associated with obesity, insulin resistance (IR), diabetes and cardiovascular diseases (CVD). Disturbances in eNOS and iNOS regulation accompany multiple changes in endothelial function and contribute to development of CVD. Furthermore, key step in initiation and progression of atherosclerosis is reduction in bioactivity of endothelial cell-derived NO. Here we shall focus on recent literature data related to the role of eNOS and iNOS in physiological and pathophysiological conditions. © 2018 Nova Science Publishers, Inc. All rights reserved.
PB  - Nova Science Publishers
T2  - Horizons in World Cardiovascular Research
T1  - The role of eNOS and iNOS in pathophysiological conditions
VL  - 15
SP  - 65
EP  - 102
ER  - 
@article{
author = "Obradović, Milan M. and Zarić, Božidarka and Sudar-Milovanović, Emina and Perović, Milan and Resanović, Ivana and Gluvić, Zoran and Isenović, Esma R.",
year = "2018",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8014",
abstract = "Nitric oxide (NO) is a free radical which, in reactions with various molecules causes multiple biological effects. NO is exceptionally regulated and extends to almost every cell type and function within circulation. Generation and actions of NO are regulated by various hormones under physiological and pathophysiological conditions. Nitric oxide synthases (NOS) are the enzymes responsible for NO generation. In mammals, neuronal NOS (nNOS) and endothelial NOS (eNOS) are constitutively expressed, while inducible NOS (iNOS) mediate in immune defense. Altered NO level is associated with obesity, insulin resistance (IR), diabetes and cardiovascular diseases (CVD). Disturbances in eNOS and iNOS regulation accompany multiple changes in endothelial function and contribute to development of CVD. Furthermore, key step in initiation and progression of atherosclerosis is reduction in bioactivity of endothelial cell-derived NO. Here we shall focus on recent literature data related to the role of eNOS and iNOS in physiological and pathophysiological conditions. © 2018 Nova Science Publishers, Inc. All rights reserved.",
publisher = "Nova Science Publishers",
journal = "Horizons in World Cardiovascular Research",
title = "The role of eNOS and iNOS in pathophysiological conditions",
volume = "15",
pages = "65-102"
}

PCSK9 and Hypercholesterolemia: Therapeutic Approach

Obradović, Milan M.; Zarić, Božidarka; Sudar-Milovanović, Emina; Ilinčić, Branislava; Stokić, Edita; Perović, Milan; Isenović, Esma R.

(2018)

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Zarić, Božidarka
AU  - Sudar-Milovanović, Emina
AU  - Ilinčić, Branislava
AU  - Stokić, Edita
AU  - Perović, Milan
AU  - Isenović, Esma R.
PY  - 2018
UR  - http://www.eurekaselect.com/158061/article
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7916
AB  - Despite the intensive research and progress in modern pharmacotherapy, hypercholesterolemia and related cardiovascular complications remain one of the leading causes of mortality and disability in the modern world. A significant contribution to the treatment of hypercholesterolemia was made by the discovery of proprotein convertase subtilisin/kexin type 9 (PCSK9). This enzyme is responsible for the degradation of the low-density lipoprotein (LDL) receptor (LDLR) found at the surface of the plasma membrane in the liver and directly associated with serum LDL level. Limitations in standard therapy used in the treatment of lipid disorders have led to the development of new drugs, such as an inhibitor of PCSK9. Over the past years, the greatest achievement in discovering the PCSK9 inhibitor was made by designing monoclonal antibodies that disable PCSK9 to bind LDLR and RNA interference to reduce PCSK9 production, but one of the main disadvantages is costeffectiveness. In this review, we will summarize the most recent findings of basic and clinical studies which focus on PCSK9 function, regulation and therapeutic target for the treatment of hypercholesterolemia and associated cardiovascular diseases.
T2  - Current Drug Targets
T1  - PCSK9 and Hypercholesterolemia: Therapeutic Approach
VL  - 19
IS  - 9
SP  - 1058
EP  - 1067
DO  - 10.2174/1389450119666171205101401
ER  - 
@article{
author = "Obradović, Milan M. and Zarić, Božidarka and Sudar-Milovanović, Emina and Ilinčić, Branislava and Stokić, Edita and Perović, Milan and Isenović, Esma R.",
year = "2018",
url = "http://www.eurekaselect.com/158061/article, http://vinar.vin.bg.ac.rs/handle/123456789/7916",
abstract = "Despite the intensive research and progress in modern pharmacotherapy, hypercholesterolemia and related cardiovascular complications remain one of the leading causes of mortality and disability in the modern world. A significant contribution to the treatment of hypercholesterolemia was made by the discovery of proprotein convertase subtilisin/kexin type 9 (PCSK9). This enzyme is responsible for the degradation of the low-density lipoprotein (LDL) receptor (LDLR) found at the surface of the plasma membrane in the liver and directly associated with serum LDL level. Limitations in standard therapy used in the treatment of lipid disorders have led to the development of new drugs, such as an inhibitor of PCSK9. Over the past years, the greatest achievement in discovering the PCSK9 inhibitor was made by designing monoclonal antibodies that disable PCSK9 to bind LDLR and RNA interference to reduce PCSK9 production, but one of the main disadvantages is costeffectiveness. In this review, we will summarize the most recent findings of basic and clinical studies which focus on PCSK9 function, regulation and therapeutic target for the treatment of hypercholesterolemia and associated cardiovascular diseases.",
journal = "Current Drug Targets",
title = "PCSK9 and Hypercholesterolemia: Therapeutic Approach",
volume = "19",
number = "9",
pages = "1058-1067",
doi = "10.2174/1389450119666171205101401"
}
1
4
3
2

IGF-1 regulates cardiac hypertrophy and inos expression in obese male rats through ERK1/2 signaling pathway

Panić, Anastasija; Stanimirović, Julijana; Obradović, Milan M.; Sudar-Milovanović, Emina; Isenović, Esma R.

(2018)

TY  - CONF
AU  - Panić, Anastasija
AU  - Stanimirović, Julijana
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Isenović, Esma R.
PY  - 2018
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0021915018307135
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7944
C3  - Atherosclerosis
T1  - IGF-1 regulates cardiac hypertrophy and inos expression in obese male rats through ERK1/2 signaling pathway
VL  - 275
SP  - e137
DO  - 10.1016/j.atherosclerosis.2018.06.401
ER  - 
@conference{
author = "Panić, Anastasija and Stanimirović, Julijana and Obradović, Milan M. and Sudar-Milovanović, Emina and Isenović, Esma R.",
year = "2018",
url = "https://linkinghub.elsevier.com/retrieve/pii/S0021915018307135, http://vinar.vin.bg.ac.rs/handle/123456789/7944",
journal = "Atherosclerosis",
title = "IGF-1 regulates cardiac hypertrophy and inos expression in obese male rats through ERK1/2 signaling pathway",
volume = "275",
pages = "e137",
doi = "10.1016/j.atherosclerosis.2018.06.401"
}

17β-estradiol inhibits hepatic iNOS via the activation of the estrogen receptor ER-α and inhibition of erk1/2-mir-221 axis

Panić, Anastasija; Stanimirović, Julijana; Obradović, Milan M.; Zafirović, Sonja; Sudar-Milovanović, Emina; Petrović, Nina; Isenović, Esma R.

(2018)

TY  - JOUR
AU  - Panić, Anastasija
AU  - Stanimirović, Julijana
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Sudar-Milovanović, Emina
AU  - Petrović, Nina
AU  - Isenović, Esma R.
PY  - 2018
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8013
AB  - 17β-Estradiol (E2) is known to negatively regulate inducible nitric oxide (NO) synthase (iNOS) expression via estrogen receptor alpha (ER-α) activation in aortic vascular smooth muscle cells.Therefore, we sought to determine whether E2 can inhibit iNOS in vivo in hepatic tissue via the activation of ER-α and whether extracellular signal-regulated kinases 1/2 (ERK1/2)-miR-221 axis is involved in this process. Male Wistar rats were treated with a bolus injection of E2 intraperitoneally (40 μg/kg), and 24 hours after treatment the animals were sacrificed and the livers excised. The protein levels of iNOS, p50 and p65 subunits of nuclear factor κB (NFκB), ERα, ERK1/2 and protein kinase B (Akt), as well as the association of ERα/Src in liver lysates were assessed by Western blot. The expression of hepatic miR-221 was analyzed by qRT-PCR. Results show that E2 reduced hepatic iNOS protein expression (p less than 0.01), the protein level of ERα (p less than 0.05), ERK1/2 (p less than 0.05), Akt phosphorylation (p less than 0.001) and miR-221 expression (p less than 0.05). In contrast, hepatic ERα/Src kinase association level (p less than 0.05) increased after E2 treatment. Our results indicate that E2 inhibits hepatic iNOS via molecular mechanisms involving the activation of the ER-α and inhibition of ERK1/2-miR-221 axis.
T2  - Journal of biological regulators and homeostatic agents
T1  - 17β-estradiol inhibits hepatic iNOS via the activation of the estrogen receptor ER-α and inhibition of erk1/2-mir-221 axis
VL  - 32
IS  - 6
SP  - 1369
EP  - 1377
ER  - 
@article{
author = "Panić, Anastasija and Stanimirović, Julijana and Obradović, Milan M. and Zafirović, Sonja and Sudar-Milovanović, Emina and Petrović, Nina and Isenović, Esma R.",
year = "2018",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8013",
abstract = "17β-Estradiol (E2) is known to negatively regulate inducible nitric oxide (NO) synthase (iNOS) expression via estrogen receptor alpha (ER-α) activation in aortic vascular smooth muscle cells.Therefore, we sought to determine whether E2 can inhibit iNOS in vivo in hepatic tissue via the activation of ER-α and whether extracellular signal-regulated kinases 1/2 (ERK1/2)-miR-221 axis is involved in this process. Male Wistar rats were treated with a bolus injection of E2 intraperitoneally (40 μg/kg), and 24 hours after treatment the animals were sacrificed and the livers excised. The protein levels of iNOS, p50 and p65 subunits of nuclear factor κB (NFκB), ERα, ERK1/2 and protein kinase B (Akt), as well as the association of ERα/Src in liver lysates were assessed by Western blot. The expression of hepatic miR-221 was analyzed by qRT-PCR. Results show that E2 reduced hepatic iNOS protein expression (p less than 0.01), the protein level of ERα (p less than 0.05), ERK1/2 (p less than 0.05), Akt phosphorylation (p less than 0.001) and miR-221 expression (p less than 0.05). In contrast, hepatic ERα/Src kinase association level (p less than 0.05) increased after E2 treatment. Our results indicate that E2 inhibits hepatic iNOS via molecular mechanisms involving the activation of the ER-α and inhibition of ERK1/2-miR-221 axis.",
journal = "Journal of biological regulators and homeostatic agents",
title = "17β-estradiol inhibits hepatic iNOS via the activation of the estrogen receptor ER-α and inhibition of erk1/2-mir-221 axis",
volume = "32",
number = "6",
pages = "1369-1377"
}
3

17 beta-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

Zafirović, Sonja; Obradović, Milan M.; Sudar, Emina; Jovanović, Aleksandra; Stanimirović, Julijana; Stewart, Alan J.; Pitt, Samantha J.; Isenović, Esma R.

(2017)

TY  - JOUR
AU  - Zafirović, Sonja
AU  - Obradović, Milan M.
AU  - Sudar, Emina
AU  - Jovanović, Aleksandra
AU  - Stanimirović, Julijana
AU  - Stewart, Alan J.
AU  - Pitt, Samantha J.
AU  - Isenović, Esma R.
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1520
AB  - The aim of this study was to investigate the in vivo effects of 17 beta-estradiol (E-2) on myocardial metabolism and inducible nitric oxide synthase (iNOS) expression/activity in obese rats. Male Wistar rats were fed with a normal or a high fat (HF) diet (42% fat) for 10 weeks. Half of the HF fed rats were treated with a single dose of E-2 while the other half were placebo-treated. 24 h after treatment animals were sacrificed. E-2 reduced cardiac free fatty acid (FFA) (p LT 0.05), L-arginine (p LT 0.01), iNOS mRNA (p LT 0.01), and protein (p LT 0.05) levels and translocation of the FFA transporter (CD36) (p LT 0.01) to the plasma membrane (PM) in HF fed rats. In contrast, Akt phosphorylation at Thr308 (p LT 0.05) and translocation of the glucose transporter GLUT4 (p LT 0.05) to the PM increased after E-2 treatment in HF rats. Our results indicate that E-2 acts via the PI3K/Akt signalling pathway to partially protect myocardial metabolism by attenuating the detrimental effects of increased iNOS expression/activity in HF fed rats. (C) 2017 Elsevier B.V. All rights reserved.
T2  - Molecular and Cellular Endocrinology
T1  - 17 beta-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats
VL  - 446
IS  - C
SP  - 12
EP  - 20
DO  - 10.1016/j.mce.2017.02.001
ER  - 
@article{
author = "Zafirović, Sonja and Obradović, Milan M. and Sudar, Emina and Jovanović, Aleksandra and Stanimirović, Julijana and Stewart, Alan J. and Pitt, Samantha J. and Isenović, Esma R.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1520",
abstract = "The aim of this study was to investigate the in vivo effects of 17 beta-estradiol (E-2) on myocardial metabolism and inducible nitric oxide synthase (iNOS) expression/activity in obese rats. Male Wistar rats were fed with a normal or a high fat (HF) diet (42% fat) for 10 weeks. Half of the HF fed rats were treated with a single dose of E-2 while the other half were placebo-treated. 24 h after treatment animals were sacrificed. E-2 reduced cardiac free fatty acid (FFA) (p LT 0.05), L-arginine (p LT 0.01), iNOS mRNA (p LT 0.01), and protein (p LT 0.05) levels and translocation of the FFA transporter (CD36) (p LT 0.01) to the plasma membrane (PM) in HF fed rats. In contrast, Akt phosphorylation at Thr308 (p LT 0.05) and translocation of the glucose transporter GLUT4 (p LT 0.05) to the PM increased after E-2 treatment in HF rats. Our results indicate that E-2 acts via the PI3K/Akt signalling pathway to partially protect myocardial metabolism by attenuating the detrimental effects of increased iNOS expression/activity in HF fed rats. (C) 2017 Elsevier B.V. All rights reserved.",
journal = "Molecular and Cellular Endocrinology",
title = "17 beta-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats",
volume = "446",
number = "C",
pages = "12-20",
doi = "10.1016/j.mce.2017.02.001"
}
5
6
6

Influence of a High-fat Diet on Cardiac iNOS in Female Rats

Jovanović, Aleksandra; Sudar, Emina; Obradović, Milan M.; Pitt, Samantha J.; Stewart, Alan J.; Zafirović, Sonja; Stanimirović, Julijana; Radak, Đorđe J.; Isenović, Esma R.

(2017)

TY  - JOUR
AU  - Jovanović, Aleksandra
AU  - Sudar, Emina
AU  - Obradović, Milan M.
AU  - Pitt, Samantha J.
AU  - Stewart, Alan J.
AU  - Zafirović, Sonja
AU  - Stanimirović, Julijana
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1678
AB  - Background: Overexpression of inducible nitric oxide synthase (iNOS) is a key link between high-fat (HF) diet induced obesity and cardiovascular disease. Oestradiol has cardioprotective effects that may be mediated through reduction of iNOS activity/expression. Methods: In the present study, female Wistar rats were fed a standard diet or a HF diet (42% fat) for 10 weeks. iNOS gene and protein expressions were measured in heart tissue. HF-fed rats exhibited a significant increase in cardiac iNOS mRNA by 695% (p LT 0.05), iNOS protein level by 248% (p LT 0.01), without changes in nitrate/nitrite levels. Expression of CD36 protein in plasma membranes was increased by 37% (p LT 0.05), while the concentration of free fatty acids (FFA) was reduced by 25% (p LT 0.01) in HF-fed rats. Expression of the p50 subunit of nuclear factor-kappa B (NF kappa B-p50) in heart was increased by 77% (p LT 0.01) in HF-fed rats. Expression of protein kinase B (Akt) and extracellular signal-regulated kinases 1/2 (ERK1/2) were unchanged between the groups. There was a significant increase in the ratio of phospho-Akt/total Akt but not for phospho-ERK1/2/total ERK1/2 in HF-fed rats. Estrogen receptor-levels (by 50%; p LT 0.05) and serum oestradiol concentrations (by 35%; p LT 0.05) were shown to be significantly reduced in HF-fed rats. Results and Conclusion: Our results revealed that a HF diet led to increased iNOS expression, most likely via a mechanism involving Akt and NF kappa B-p50 proteins. Decreased levels of oestradiol and ER protein in the HF-fed group, in combination with increased iNOS levels are consistent with the hypothesis that oestradiol has a cardioprotective effect through its ability to regulate iNOS expression.
T2  - Current Vascular Pharmacology
T1  - Influence of a High-fat Diet on Cardiac iNOS in Female Rats
VL  - 15
IS  - 5
SP  - 491
EP  - 500
DO  - 10.2174/1570161114666161025101303
ER  - 
@article{
author = "Jovanović, Aleksandra and Sudar, Emina and Obradović, Milan M. and Pitt, Samantha J. and Stewart, Alan J. and Zafirović, Sonja and Stanimirović, Julijana and Radak, Đorđe J. and Isenović, Esma R.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1678",
abstract = "Background: Overexpression of inducible nitric oxide synthase (iNOS) is a key link between high-fat (HF) diet induced obesity and cardiovascular disease. Oestradiol has cardioprotective effects that may be mediated through reduction of iNOS activity/expression. Methods: In the present study, female Wistar rats were fed a standard diet or a HF diet (42% fat) for 10 weeks. iNOS gene and protein expressions were measured in heart tissue. HF-fed rats exhibited a significant increase in cardiac iNOS mRNA by 695% (p LT 0.05), iNOS protein level by 248% (p LT 0.01), without changes in nitrate/nitrite levels. Expression of CD36 protein in plasma membranes was increased by 37% (p LT 0.05), while the concentration of free fatty acids (FFA) was reduced by 25% (p LT 0.01) in HF-fed rats. Expression of the p50 subunit of nuclear factor-kappa B (NF kappa B-p50) in heart was increased by 77% (p LT 0.01) in HF-fed rats. Expression of protein kinase B (Akt) and extracellular signal-regulated kinases 1/2 (ERK1/2) were unchanged between the groups. There was a significant increase in the ratio of phospho-Akt/total Akt but not for phospho-ERK1/2/total ERK1/2 in HF-fed rats. Estrogen receptor-levels (by 50%; p LT 0.05) and serum oestradiol concentrations (by 35%; p LT 0.05) were shown to be significantly reduced in HF-fed rats. Results and Conclusion: Our results revealed that a HF diet led to increased iNOS expression, most likely via a mechanism involving Akt and NF kappa B-p50 proteins. Decreased levels of oestradiol and ER protein in the HF-fed group, in combination with increased iNOS levels are consistent with the hypothesis that oestradiol has a cardioprotective effect through its ability to regulate iNOS expression.",
journal = "Current Vascular Pharmacology",
title = "Influence of a High-fat Diet on Cardiac iNOS in Female Rats",
volume = "15",
number = "5",
pages = "491-500",
doi = "10.2174/1570161114666161025101303"
}
10
8
10

Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet

Jovanović, Aleksandra; Obradović, Milan M.; Sudar, Emina; Stewart, Alan J.; Pitt, Samantha J.; Alavantić, Dragan; Aleksić, Ema; Isenović, Esma R.

(2017)

TY  - JOUR
AU  - Jovanović, Aleksandra
AU  - Obradović, Milan M.
AU  - Sudar, Emina
AU  - Stewart, Alan J.
AU  - Pitt, Samantha J.
AU  - Alavantić, Dragan
AU  - Aleksić, Ema
AU  - Isenović, Esma R.
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1812
AB  - The aim of this study was to investigate whether the presence of endogenous estradiol alters the effects of a high-fat (HF) diet on activity/expression of the cardiac Na+/K+-ATPase, via PI3K/IRS and RhoA/ROCK signalling cascades in female rats. For this study, female Wistar rats (8 weeks old, 150-200 g) were fed a standard diet or a HF diet (balanced diet for laboratory rats enriched with 42% fat) for 10 weeks. The results show that rats fed a HF diet exhibited a decrease in phosphorylation of the alpha(1) subunit of Na+/K+-ATPase by 30% (p LT 0.05), expression of total alpha(1) subunit of Na+/K+-ATPase by 31% (p LT 0.05), and association of IRS1 with p85 subunit of PI3K by 42% (p LT 0.05), while the levels of cardiac RhoA and ROCK2 were significantly increased by 84% (p LT 0.01) and 62% (p LT 0.05), respectively. Our results suggest that a HF diet alters cardiac Na+/K+-ATPase expression via molecular mechanisms involving RhoA/ROCK and IRS-1/PI3K signalling in female rats.
T2  - Molecular and Cellular Biochemistry
T1  - Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet
VL  - 436
IS  - 1-2
SP  - 49
EP  - 58
DO  - 10.1007/s11010-017-3077-y
ER  - 
@article{
author = "Jovanović, Aleksandra and Obradović, Milan M. and Sudar, Emina and Stewart, Alan J. and Pitt, Samantha J. and Alavantić, Dragan and Aleksić, Ema and Isenović, Esma R.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1812",
abstract = "The aim of this study was to investigate whether the presence of endogenous estradiol alters the effects of a high-fat (HF) diet on activity/expression of the cardiac Na+/K+-ATPase, via PI3K/IRS and RhoA/ROCK signalling cascades in female rats. For this study, female Wistar rats (8 weeks old, 150-200 g) were fed a standard diet or a HF diet (balanced diet for laboratory rats enriched with 42% fat) for 10 weeks. The results show that rats fed a HF diet exhibited a decrease in phosphorylation of the alpha(1) subunit of Na+/K+-ATPase by 30% (p LT 0.05), expression of total alpha(1) subunit of Na+/K+-ATPase by 31% (p LT 0.05), and association of IRS1 with p85 subunit of PI3K by 42% (p LT 0.05), while the levels of cardiac RhoA and ROCK2 were significantly increased by 84% (p LT 0.01) and 62% (p LT 0.05), respectively. Our results suggest that a HF diet alters cardiac Na+/K+-ATPase expression via molecular mechanisms involving RhoA/ROCK and IRS-1/PI3K signalling in female rats.",
journal = "Molecular and Cellular Biochemistry",
title = "Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet",
volume = "436",
number = "1-2",
pages = "49-58",
doi = "10.1007/s11010-017-3077-y"
}

Apoptosis and Acute Brain Ischemia in Ischemic Stroke

Radak, Đorđe J.; Katsiki, Niki; Resanović, Ivana; Jovanović, Aleksandra; Sudar, Emina; Zafirović, Sonja; Mousa, Shaker A.; Isenović, Esma R.

(2017)

@article{
author = "Radak, Đorđe J. and Katsiki, Niki and Resanović, Ivana and Jovanović, Aleksandra and Sudar, Emina and Zafirović, Sonja and Mousa, Shaker A. and Isenović, Esma R.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1521",
abstract = "Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered.",
journal = "Current Vascular Pharmacology",
title = "Apoptosis and Acute Brain Ischemia in Ischemic Stroke",
volume = "15",
number = "2",
pages = "115-122",
doi = "10.2174/1570161115666161104095522"
}
97
86
100

Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases

Obradović, Milan M.; Stanimirović, Julijana; Panić, Anastasija; Bogdanović, Nikola; Sudar, Emina; Cenic-Milosevic, Desanka; Isenović, Esma R.

(2017)

@article{
author = "Obradović, Milan M. and Stanimirović, Julijana and Panić, Anastasija and Bogdanović, Nikola and Sudar, Emina and Cenic-Milosevic, Desanka and Isenović, Esma R.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1581",
abstract = "Background: The sodium/potassium- adenosine- triphosphatase (Na+/K+-ATPase) is an important mediator in vasculature tone and contractility, and its abnormal regulation has been implicated in many diseases such as obesity, insulin resistance, diabetes, and hypertension. Decreased Na+/K+-ATPase abundance and its altered isoform expression induce cardiomyocytes death and cardiac dysfunction, possibly leading to the development of myocardial dilation and heart failure. Therefore, the regulation of Na+/K+-ATPase activity/expression could be important in treatment and possible prevention of cardio-metabolic diseases. A number of hormones and environmental factors regulate the function of Na+/K+-ATPase in response to changing cellular requirements. Estradiol and insulin like growth factor-1 (IGF-1) are among potent hormones that positively regulate Na+/K+-ATPase activity or de novo synthesis of alpha -and beta -subunits. Both estradiol and IGF-1 have a huge therapeutic potential in treatment of vasculopathy in cardio-metabolic diseases. Methods: We searched the MEDLINE and PUBMED databases for all English and non-English articles with an English abstract from April 1978 to May 2016. The main data search terms were: Na+/K+-ATPase; estradiol and Na+/K+-ATPase; estradiol, Na+/K+-ATPase and CVS; estradiol, Na+/K+-ATPase and CVD; estradiol, Na+/K+-ATPase and obesity; estradiol, Na+/K+-ATPase and diabetes; estradiol, Na+/K+-ATPase and hypertension; IGF-1; IGF-1 and Na+/K+-ATPase; IGF-1, Na+/K+-ATPase and CVS; IGF-1, Na+/K+-ATPase and CVD; IGF-1, Na+/K+-ATPase and obesity; IGF-1, Na+/K+-ATPase and diabetes; IGF-1, Na+/K+-ATPase and hypertension. Results: The present review discusses the latest data from animal and human studies which focus on the effects of estradiol and IGF-1 on Na+/K+-ATPase regulation in physiological and pathophysiological conditions in cardiovascular system. Conclusion: Understanding the molecular mechanisms of estradiol and IGF-1 action on Na+/K+-ATPase in humans, may help resolving outstanding issues and developing new strategies for the protection and treatment of cardiovascular diseases.",
journal = "Current Pharmaceutical Design",
title = "Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases",
volume = "23",
number = "10",
pages = "1551-1561",
doi = "10.2174/1381612823666170203113455"
}
6
6
6

Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases

Sudar, Emina; Zafirović, Sonja; Jovanović, Aleksandra; Trebaljevac, Jovana; Obradović, Milan M.; Cenic-Milosevic, Desanka; Isenović, Esma R.

(2017)

@article{
author = "Sudar, Emina and Zafirović, Sonja and Jovanović, Aleksandra and Trebaljevac, Jovana and Obradović, Milan M. and Cenic-Milosevic, Desanka and Isenović, Esma R.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1580",
abstract = "Background: Nitric oxide (NO) is a potential biochemical, cardio-metabolic risk marker. The production of NO is catalyzed by different isoforms of enzymes, NO synthases (NOS). An altered NO level is associated with obesity, insulin resistance (IR), diabetes and cardiovascular diseases (CVD). Activity of NOS and NO production are regulated by various hormones under physiological and pathophysiological condition. Methods: Data used for this review were obtained by searching the electronic database [PUBMED/MEDLINE 1984 - May 2016]. Additionally, abstracts from national and international diabetes and cardiovascular related meetings were searched. The main data search terms were: nitric oxide, nitric oxide synthase, cardio-metabolic risk, obesity, diabetes, cardiovascular disease, estradiol and insulin-like growth factor-1. Results: In this review, we summarize the recent literature data related to the regulation of endothelial NOS (eNOS), inducible (iNOS) activity/expression, and thereby NO production by the hormones: estradiol (E2), and insulin-like growth factor-1 (IGF-1). Conclusion: Understanding the regulation of NO production by different hormones such as E2, and IGF-1 may provide novel and useful knowledge regarding how endothelial dysfunction (ED) is linked with cardio-metabolic alterations and diseases.",
journal = "Current Pharmaceutical Design",
title = "Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases",
volume = "23",
number = "10",
pages = "1427-1434",
doi = "10.2174/1381612823666170124124855"
}
4
3
7

Benefits of L-Arginine on Cardiovascular System

Sudar, Emina; Obradović, Milan M.; Jovanović, Aleksandra; Zarić, Božidarka; Zafirović, Sonja; Panić, Anastasija; Radak, Đorđe J.; Isenović, Esma R.

(2016)

@article{
author = "Sudar, Emina and Obradović, Milan M. and Jovanović, Aleksandra and Zarić, Božidarka and Zafirović, Sonja and Panić, Anastasija and Radak, Đorđe J. and Isenović, Esma R.",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/829",
abstract = "The amino acid, L-Arginine (L-Arg) plays an important role in the cardiovascular system. Data from the literature show that L-Arg is the only substrate for the production of nitric oxide (NO), from which L-Arg develops its effects on the cardiovascular system. As a free radical, NO is synthesized in all mammalian cells by L-Arg with the activity of NO synthase (NOS). In states of hypertension, diabetes, hypercholesterolemia and vascular inflammation a disorder occurs in the metabolic pathway of the synthesis of NO from L-Arg which all together bring alterations of blood vessels. Experimental results obtained on animals, as well as clinical studies show that L-Arg has an effect on thrombocytes, on the process of coagulation and on the fibrolytic system. This mini review represents a summary of the latest scientific animal and human studies related to L-Arg and its mechanisms of actions with a focus on the role of L-Arg via NO pathway in cardiovascular disorders. Moreover, here we present data from recent animal and clinical studies suggesting that L-Arg could be one of the possible therapeutic molecules for improving the treatment of different cardiovascular disorders.",
journal = "Mini Reviews in Medicinal Chemistry",
title = "Benefits of L-Arginine on Cardiovascular System",
volume = "16",
number = "2",
pages = "94-103",
doi = "10.2174/1389557515666151016125826"
}
10
8
10

Treatment of Alzheimers Disease: Classical Therapeutic Approach

Bajić, Vladan P.; Sudar, Emina; Spremo-Potparević, Biljana; Živković, Lada; Milićević, Zorka T.; Stanimirović, Julijana; Bogdanović, Nikola; Isenović, Esma R.

(2016)

TY  - JOUR
AU  - Bajić, Vladan P.
AU  - Sudar, Emina
AU  - Spremo-Potparević, Biljana
AU  - Živković, Lada
AU  - Milićević, Zorka T.
AU  - Stanimirović, Julijana
AU  - Bogdanović, Nikola
AU  - Isenović, Esma R.
PY  - 2016
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1039
AB  - Alzheimers disease (AD) is a complex and progressive neurodegenerative disorder, and represents the most common form of dementia. The number of people affected by AD is estimated to be doubled by the year of 2050, and more than 100 million people worldwide will be affected by this disease. Still, there is no reliable diagnostic test which would indicate pre-symptomatic conditions or an increased risk of developing AD. The only drugs approved by the FDA belong to the cholinesterase inhibitors (ChEI) group, such as donepezil, rivastigmine, galantamine and memantine that belongs to a class of drugs named receptor NMDA antagonists. Most mainstream pharmacotherapeutic approaches act by slowing the progression of the condition rather than to treat or prevent the cause of AD. In this review we are presenting literature data from recent research related to new avenues in the classical approach to prevention and treatment of AD.
T2  - Current Pharmaceutical Analysis
T1  - Treatment of Alzheimers Disease: Classical Therapeutic Approach
VL  - 12
IS  - 2
SP  - 82
EP  - 90
DO  - 10.2174/1573412911666150611184740
ER  - 
@article{
author = "Bajić, Vladan P. and Sudar, Emina and Spremo-Potparević, Biljana and Živković, Lada and Milićević, Zorka T. and Stanimirović, Julijana and Bogdanović, Nikola and Isenović, Esma R.",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1039",
abstract = "Alzheimers disease (AD) is a complex and progressive neurodegenerative disorder, and represents the most common form of dementia. The number of people affected by AD is estimated to be doubled by the year of 2050, and more than 100 million people worldwide will be affected by this disease. Still, there is no reliable diagnostic test which would indicate pre-symptomatic conditions or an increased risk of developing AD. The only drugs approved by the FDA belong to the cholinesterase inhibitors (ChEI) group, such as donepezil, rivastigmine, galantamine and memantine that belongs to a class of drugs named receptor NMDA antagonists. Most mainstream pharmacotherapeutic approaches act by slowing the progression of the condition rather than to treat or prevent the cause of AD. In this review we are presenting literature data from recent research related to new avenues in the classical approach to prevention and treatment of AD.",
journal = "Current Pharmaceutical Analysis",
title = "Treatment of Alzheimers Disease: Classical Therapeutic Approach",
volume = "12",
number = "2",
pages = "82-90",
doi = "10.2174/1573412911666150611184740"
}
13
9
10

A high fat diet induces sex-specific differences in hepatic lipid metabolism and nitrite/nitrate in rats

Stanimirović, Julijana; Obradović, Milan M.; Jovanović, Aleksandra; Sudar, Emina; Zafirović, Sonja; Pitt, Samantha J.; Stewart, Alan J.; Isenović, Esma R.

(2016)

TY  - JOUR
AU  - Stanimirović, Julijana
AU  - Obradović, Milan M.
AU  - Jovanović, Aleksandra
AU  - Sudar, Emina
AU  - Zafirović, Sonja
AU  - Pitt, Samantha J.
AU  - Stewart, Alan J.
AU  - Isenović, Esma R.
PY  - 2016
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1004
AB  - Men and women differ substantially with regard to the severity of insulin resistance (IR) but the underlying mechanism(s) of how this occurs is poorly characterized. We investigated whether a high fat (HF) diet resulted in sex-specific differences in nitrite/nitrate production and lipid metabolism and whether these variances may contribute to altered obesity-induced IR. Male and female Wistar rats were fed a standard laboratory diet or a HF diet for 10 weeks. The level of plasma nitrite/nitrate, as well as free fatty acid (FFA), in both plasma and liver lysates were assessed. The levels of inducible nitric oxide (NO) synthase (iNOS), p65 subunit of NF kappa B, total and phosphorylated forms of Akt, mTOR and PDK-1 in lysates, and the levels of glucose transporter 2 (Glut-2) and fatty acid translocase/cluster of differentiation 36 (FAT/CD36) in plasma membrane fractions of liver were assessed. HF-fed male rats exhibited a significant increase in plasma nitrite/nitrate, and hepatic FFA and FAT/CD36 levels compared with controls. They also displayed a relative decrease in iNOS and Glut-2 levels in the liver. Phosphorylation of Akt (at Ser(473) and Thr(308)), mTOR and PDK-1 was also reduced. HF-fed female rats exhibited increased levels of NF kappa B-p65 in liver compared with controls, while levels of Glut-2, FAT/CD36 and Akt phosphorylation at Thr(308) and PDK-1 were decreased. Our results reveal that altered lipid and glucose metabolism in obesity, lead to altered iNOS expression and nitrite/nitrate production. It is likely that this mechanism contributes to sex-specific differences in the development of IR. (C) 2016 Elsevier Inc. All rights reserved.
T2  - Nitric Oxide: Biology and Chemistry
T1  - A high fat diet induces sex-specific differences in hepatic lipid metabolism and nitrite/nitrate in rats
VL  - 54
SP  - 51
EP  - 59
DO  - 10.1016/j.niox.2016.02.007
ER  - 
@article{
author = "Stanimirović, Julijana and Obradović, Milan M. and Jovanović, Aleksandra and Sudar, Emina and Zafirović, Sonja and Pitt, Samantha J. and Stewart, Alan J. and Isenović, Esma R.",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1004",
abstract = "Men and women differ substantially with regard to the severity of insulin resistance (IR) but the underlying mechanism(s) of how this occurs is poorly characterized. We investigated whether a high fat (HF) diet resulted in sex-specific differences in nitrite/nitrate production and lipid metabolism and whether these variances may contribute to altered obesity-induced IR. Male and female Wistar rats were fed a standard laboratory diet or a HF diet for 10 weeks. The level of plasma nitrite/nitrate, as well as free fatty acid (FFA), in both plasma and liver lysates were assessed. The levels of inducible nitric oxide (NO) synthase (iNOS), p65 subunit of NF kappa B, total and phosphorylated forms of Akt, mTOR and PDK-1 in lysates, and the levels of glucose transporter 2 (Glut-2) and fatty acid translocase/cluster of differentiation 36 (FAT/CD36) in plasma membrane fractions of liver were assessed. HF-fed male rats exhibited a significant increase in plasma nitrite/nitrate, and hepatic FFA and FAT/CD36 levels compared with controls. They also displayed a relative decrease in iNOS and Glut-2 levels in the liver. Phosphorylation of Akt (at Ser(473) and Thr(308)), mTOR and PDK-1 was also reduced. HF-fed female rats exhibited increased levels of NF kappa B-p65 in liver compared with controls, while levels of Glut-2, FAT/CD36 and Akt phosphorylation at Thr(308) and PDK-1 were decreased. Our results reveal that altered lipid and glucose metabolism in obesity, lead to altered iNOS expression and nitrite/nitrate production. It is likely that this mechanism contributes to sex-specific differences in the development of IR. (C) 2016 Elsevier Inc. All rights reserved.",
journal = "Nitric Oxide: Biology and Chemistry",
title = "A high fat diet induces sex-specific differences in hepatic lipid metabolism and nitrite/nitrate in rats",
volume = "54",
pages = "51-59",
doi = "10.1016/j.niox.2016.02.007"
}
3
18
20
23

Nitric Oxide as a Marker for Levo-Thyroxine Therapy in Subclinical Hypothyroid Patients

Obradović, Milan M.; Gluvić, Zoran; Sudar, Emina; Panić, Anastasija; Trebaljevac, Jovana; Bajić, Vladan P.; Zarkovic, Milos; Isenović, Esma R.

(2016)

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Gluvić, Zoran
AU  - Sudar, Emina
AU  - Panić, Anastasija
AU  - Trebaljevac, Jovana
AU  - Bajić, Vladan P.
AU  - Zarkovic, Milos
AU  - Isenović, Esma R.
PY  - 2016
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1006
AB  - Subclinical hypothyroidism (SH) is characterized by a mildly elevated concentration of thyroid stimulating hormone (TSH) despite free thyroxine (FT4) and triiodothyronine (FT3) levels within the reference range. Numerous studies revealed SH to be an independent risk factor for cardiovascular disease (CVD),including atherosclerosis, congestive heart failure, coronary heart disease, ischemic heart disease and the associated mortality. The relationship between SH and CVD is well documented, but the molecular mechanism underlying this correlation remain unknown. Endothelial dysfunction has been recognized as an initial step leading to CVD in patients with SH. Changes in lipid profile, inflammation and/or oxidative stress contribute to the endothelial dysfunction in SH. Moreover, the progression of SH is characterized by significantly decreased nitrite and nitrate levels. Recent animal and clinical studies discussed in this review suggest that nitric oxide (NO) levels could be a reliable biomarker for cardiovascular risk in SH. Understanding the regulation of NO production by thyroid hormone may provide novel and useful knowledge regarding how endothelial dysfunction in SH is linked with CVD and help us to uncover new treatments for SH. We suggest that serum NO level may be an indicator for the introduction and dosage of levothyroxine (LT4) replacement therapy in SH patients. Future studies should focus on understanding the molecular mechanisms underlying the effects of NO in physiological as well as in pathophysiological conditions such as hypothyroidism and their clinical relevance.
T2  - Current Vascular Pharmacology
T1  - Nitric Oxide as a Marker for Levo-Thyroxine Therapy in Subclinical Hypothyroid Patients
VL  - 14
IS  - 3
SP  - 266
EP  - 270
DO  - 10.2174/1570161114666160208143537
ER  - 
@article{
author = "Obradović, Milan M. and Gluvić, Zoran and Sudar, Emina and Panić, Anastasija and Trebaljevac, Jovana and Bajić, Vladan P. and Zarkovic, Milos and Isenović, Esma R.",
year = "2016",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1006",
abstract = "Subclinical hypothyroidism (SH) is characterized by a mildly elevated concentration of thyroid stimulating hormone (TSH) despite free thyroxine (FT4) and triiodothyronine (FT3) levels within the reference range. Numerous studies revealed SH to be an independent risk factor for cardiovascular disease (CVD),including atherosclerosis, congestive heart failure, coronary heart disease, ischemic heart disease and the associated mortality. The relationship between SH and CVD is well documented, but the molecular mechanism underlying this correlation remain unknown. Endothelial dysfunction has been recognized as an initial step leading to CVD in patients with SH. Changes in lipid profile, inflammation and/or oxidative stress contribute to the endothelial dysfunction in SH. Moreover, the progression of SH is characterized by significantly decreased nitrite and nitrate levels. Recent animal and clinical studies discussed in this review suggest that nitric oxide (NO) levels could be a reliable biomarker for cardiovascular risk in SH. Understanding the regulation of NO production by thyroid hormone may provide novel and useful knowledge regarding how endothelial dysfunction in SH is linked with CVD and help us to uncover new treatments for SH. We suggest that serum NO level may be an indicator for the introduction and dosage of levothyroxine (LT4) replacement therapy in SH patients. Future studies should focus on understanding the molecular mechanisms underlying the effects of NO in physiological as well as in pathophysiological conditions such as hypothyroidism and their clinical relevance.",
journal = "Current Vascular Pharmacology",
title = "Nitric Oxide as a Marker for Levo-Thyroxine Therapy in Subclinical Hypothyroid Patients",
volume = "14",
number = "3",
pages = "266-270",
doi = "10.2174/1570161114666160208143537"
}
14
12
17

Non-Classical Therapeutic Approach in the Treatment of Alzheimers Disease: A Mini Review

Bajić, Vladan P.; Spremo-Potparević, Biljana; Živković, Lada; Sudar, Emina; Zafirović, Sonja; Obradović, Milan M.; Isenović, Esma R.

(2015)

TY  - JOUR
AU  - Bajić, Vladan P.
AU  - Spremo-Potparević, Biljana
AU  - Živković, Lada
AU  - Sudar, Emina
AU  - Zafirović, Sonja
AU  - Obradović, Milan M.
AU  - Isenović, Esma R.
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/398
AB  - Alzheimers disease (AD) is a multi factorial disease, related to the loss of neurons and synapses in cerebral cortex and subcortical structures, leading to degenerative changes and atrophy. Despite abundance of facts related to AD and its pathology, the only drugs used in the prevention and treatment are those from the cholinesterase inhibitors group. However, there is growing evidence that a non-classical therapeutic approach in the treatment of AD has beneficial effects. In this review we summarized recent literature data related to the non-classical drugs for the treatment of AD predominantly used in clinical testing, such as amyloid aggregation inhibitors, beta-sheet breakers, antioxidants, estrogens and immunotherapeutics.
T2  - Letters in Drug Design and Discovery
T1  - Non-Classical Therapeutic Approach in the Treatment of Alzheimers Disease: A Mini Review
VL  - 12
IS  - 2
SP  - 158
EP  - 164
ER  - 
@article{
author = "Bajić, Vladan P. and Spremo-Potparević, Biljana and Živković, Lada and Sudar, Emina and Zafirović, Sonja and Obradović, Milan M. and Isenović, Esma R.",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/398",
abstract = "Alzheimers disease (AD) is a multi factorial disease, related to the loss of neurons and synapses in cerebral cortex and subcortical structures, leading to degenerative changes and atrophy. Despite abundance of facts related to AD and its pathology, the only drugs used in the prevention and treatment are those from the cholinesterase inhibitors group. However, there is growing evidence that a non-classical therapeutic approach in the treatment of AD has beneficial effects. In this review we summarized recent literature data related to the non-classical drugs for the treatment of AD predominantly used in clinical testing, such as amyloid aggregation inhibitors, beta-sheet breakers, antioxidants, estrogens and immunotherapeutics.",
journal = "Letters in Drug Design and Discovery",
title = "Non-Classical Therapeutic Approach in the Treatment of Alzheimers Disease: A Mini Review",
volume = "12",
number = "2",
pages = "158-164"
}
3