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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

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info:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173033/RS//

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 (en)
Хормонска регулација експресије и активности азот оксид синтазе и натријум-калијумове пумпе у експерименталним моделима инсулинске резистенције, дијабетеса и кардиоваскуларних поремећаја (sr)
Hormonska regulacija ekspresije i aktivnosti azot oksid sintaze i natrijum-kalijumove pumpe u eksperimentalnim modelima insulinske rezistencije, dijabetesa i kardiovaskularnih poremećaja (sr_RS)

Publications

The X Files: “The Mystery of X Chromosome Instability in Alzheimer’s Disease”

Bajić, Vladan P.; Essack, Magbubah; Živković, Lada; Stewart, Alan J.; Zafirović, Sonja; Bajić, Vladimir B.; Gojobori, Takashi; Isenović, Esma R.; Spremo-Potparević, Biljana

(2020)

TY  - JOUR
AU  - Bajić, Vladan P.
AU  - Essack, Magbubah
AU  - Živković, Lada
AU  - Stewart, Alan J.
AU  - Zafirović, Sonja
AU  - Bajić, Vladimir B.
AU  - Gojobori, Takashi
AU  - Isenović, Esma R.
AU  - Spremo-Potparević, Biljana
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8825
AB  - Alzheimer’s disease (AD) is a neurodegenerative disease that affects millions of individuals worldwide and can occur relatively early or later in life. It is well known that genetic components, such as the amyloid precursor protein gene on chromosome 21, are fundamental in early-onset AD (EOAD). To date, however, only the apolipoprotein E4 (ApoE4) gene has been proved to be a genetic risk factor for late-onset AD (LOAD). In recent years, despite the hypothesis that many additional unidentified genes are likely to play a role in AD development, it is surprising that additional gene polymorphisms associated with LOAD have failed to come to light. In this review, we examine the role of X chromosome epigenetics and, based upon GWAS studies, the PCDHX11 gene. Furthermore, we explore other genetic risk factors of AD that involve X-chromosome epigenetics. © Copyright © 2020 Bajic, Essack, Zivkovic, Stewart, Zafirovic, Bajic, Gojobori, Isenovic and Spremo-Potparevic.
T2  - Frontiers in Genetics
T1  - The X Files: “The Mystery of X Chromosome Instability in Alzheimer’s Disease”
VL  - 10
DO  - 10.3389/fgene.2019.01368
ER  - 
@article{
author = "Bajić, Vladan P. and Essack, Magbubah and Živković, Lada and Stewart, Alan J. and Zafirović, Sonja and Bajić, Vladimir B. and Gojobori, Takashi and Isenović, Esma R. and Spremo-Potparević, Biljana",
year = "2020",
url = "https://vinar.vin.bg.ac.rs/handle/123456789/8825",
abstract = "Alzheimer’s disease (AD) is a neurodegenerative disease that affects millions of individuals worldwide and can occur relatively early or later in life. It is well known that genetic components, such as the amyloid precursor protein gene on chromosome 21, are fundamental in early-onset AD (EOAD). To date, however, only the apolipoprotein E4 (ApoE4) gene has been proved to be a genetic risk factor for late-onset AD (LOAD). In recent years, despite the hypothesis that many additional unidentified genes are likely to play a role in AD development, it is surprising that additional gene polymorphisms associated with LOAD have failed to come to light. In this review, we examine the role of X chromosome epigenetics and, based upon GWAS studies, the PCDHX11 gene. Furthermore, we explore other genetic risk factors of AD that involve X-chromosome epigenetics. © Copyright © 2020 Bajic, Essack, Zivkovic, Stewart, Zafirovic, Bajic, Gojobori, Isenovic and Spremo-Potparevic.",
journal = "Frontiers in Genetics",
title = "The X Files: “The Mystery of X Chromosome Instability in Alzheimer’s Disease”",
volume = "10",
doi = "10.3389/fgene.2019.01368"
}
13
1
1

Endothelial dysfunction in dyslipidaemia: Molecular mechanisms and clinical implications

Zarić, Božidarka; Obradović, Milan M.; Trpković, Andreja; Banach, Maciej; Mikhailidis, Dimitri P.; Isenović, Esma R.

(2020)

TY  - JOUR
AU  - Zarić, Božidarka
AU  - Obradović, Milan M.
AU  - Trpković, Andreja
AU  - Banach, Maciej
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8811
AB  - The endothelium consists of a monolayer of Endothelial Cells (ECs) which form the inner cellular lining of veins, arteries, capillaries and lymphatic vessels. ECs interact with the blood and lymph. The endothelium fulfils functions such as vasodilatation, regulation of adhesion, infiltration of leukocytes, inhibition of platelet adhesion, vessel remodeling and lipoprotein metabolism. ECs synthesize and release compounds such as Nitric Oxide (NO), metabolites of arachidonic acid, Reactive Oxygen Species (ROS) and enzymes that degrade the extracellular matrix. Endothelial dysfunction represents a phenotype prone to atherogenesis and may be used as a marker of atherosclerotic risk. Such dysfunction includes impaired synthesis and availability of NO and an imbalance in the relative contribution of endothelial-derived relaxing factors and contracting factors such as endothelin-1 and angiotensin. This dysfunction appears before the earliest anatomic evidence of atherosclerosis and could be an important initial step in further development of atherosclerosis. Endothelial dysfunction was historically treated with vitamin C supplementation and L-arginine supplementation. Short term improvement of the expression of adhesion molecule and endothelial function during antioxidant therapy has been observed. Statins are used in the treatment of hyperlipidaemia, a risk factor for cardiovascular disease. Future studies should focus on identifying the mechanisms involved in the beneficial effects of statins on the endothelium. This may help develop drugs specifically aimed at endothelial dysfunction. © 2020 Bentham Science Publishers.
T2  - Current Medicinal Chemistry
T1  - Endothelial dysfunction in dyslipidaemia: Molecular mechanisms and clinical implications
VL  - 27
IS  - 7
SP  - 1021
EP  - 1040
DO  - 10.2174/0929867326666190903112146
ER  - 
@article{
author = "Zarić, Božidarka and Obradović, Milan M. and Trpković, Andreja and Banach, Maciej and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2020",
url = "https://vinar.vin.bg.ac.rs/handle/123456789/8811",
abstract = "The endothelium consists of a monolayer of Endothelial Cells (ECs) which form the inner cellular lining of veins, arteries, capillaries and lymphatic vessels. ECs interact with the blood and lymph. The endothelium fulfils functions such as vasodilatation, regulation of adhesion, infiltration of leukocytes, inhibition of platelet adhesion, vessel remodeling and lipoprotein metabolism. ECs synthesize and release compounds such as Nitric Oxide (NO), metabolites of arachidonic acid, Reactive Oxygen Species (ROS) and enzymes that degrade the extracellular matrix. Endothelial dysfunction represents a phenotype prone to atherogenesis and may be used as a marker of atherosclerotic risk. Such dysfunction includes impaired synthesis and availability of NO and an imbalance in the relative contribution of endothelial-derived relaxing factors and contracting factors such as endothelin-1 and angiotensin. This dysfunction appears before the earliest anatomic evidence of atherosclerosis and could be an important initial step in further development of atherosclerosis. Endothelial dysfunction was historically treated with vitamin C supplementation and L-arginine supplementation. Short term improvement of the expression of adhesion molecule and endothelial function during antioxidant therapy has been observed. Statins are used in the treatment of hyperlipidaemia, a risk factor for cardiovascular disease. Future studies should focus on identifying the mechanisms involved in the beneficial effects of statins on the endothelium. This may help develop drugs specifically aimed at endothelial dysfunction. © 2020 Bentham Science Publishers.",
journal = "Current Medicinal Chemistry",
title = "Endothelial dysfunction in dyslipidaemia: Molecular mechanisms and clinical implications",
volume = "27",
number = "7",
pages = "1021-1040",
doi = "10.2174/0929867326666190903112146"
}
5
4
3

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

Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy

Obradović, Milan M.; Zafirović, Sonja; Essack, Magbubah; Dimitrov, Jelena; Živković, Lada; Spremo-Potparević, Biljana; Radak, Đorđe J.; Bajić, Vladimir B.; Isenović, Esma R.

(Churchill Livingstone, 2020)

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Essack, Magbubah
AU  - Dimitrov, Jelena
AU  - Živković, Lada
AU  - Spremo-Potparević, Biljana
AU  - Radak, Đorđe J.
AU  - Bajić, Vladimir B.
AU  - Isenović, Esma R.
PY  - 2020
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8487
AB  - To remedy carotid artery stenosis and prevent stroke surgical intervention is commonly used, and the gold standard being carotid endarterectomy (CEA). During CEA cerebrovascular hemoglobin oxygen saturation decreases and when this decrease reaches critical levels it leads to cerebral hypoxia that causes neuronal damage. One of the proposed mechanism that affects changes during CEA and contribute to acute brain ischemia (ABI) is oxidative stress. The increased production of reactive oxygen species and reactive nitrogen species during ABI may cause an unregulated inflammatory response and further lead to structural and functional injury of neurons. Antioxidant activity are involved in the protection against neuronal damage after cerebral ischemia. We hypothesized that neuronal injury and poor outcomes in patients undergoing CEA may be results of oxidative stress that disturbed function of antioxidant enzymes and contributed to the DNA damage in lymphocytes. © 2019 The Authors
PB  - Churchill Livingstone
T2  - Medical Hypotheses
T1  - Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy
VL  - 134
SP  - 109419
DO  - 10.1016/j.mehy.2019.109419
ER  - 
@article{
author = "Obradović, Milan M. and Zafirović, Sonja and Essack, Magbubah and Dimitrov, Jelena and Živković, Lada and Spremo-Potparević, Biljana and Radak, Đorđe J. and Bajić, Vladimir B. and Isenović, Esma R.",
year = "2020",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8487",
abstract = "To remedy carotid artery stenosis and prevent stroke surgical intervention is commonly used, and the gold standard being carotid endarterectomy (CEA). During CEA cerebrovascular hemoglobin oxygen saturation decreases and when this decrease reaches critical levels it leads to cerebral hypoxia that causes neuronal damage. One of the proposed mechanism that affects changes during CEA and contribute to acute brain ischemia (ABI) is oxidative stress. The increased production of reactive oxygen species and reactive nitrogen species during ABI may cause an unregulated inflammatory response and further lead to structural and functional injury of neurons. Antioxidant activity are involved in the protection against neuronal damage after cerebral ischemia. We hypothesized that neuronal injury and poor outcomes in patients undergoing CEA may be results of oxidative stress that disturbed function of antioxidant enzymes and contributed to the DNA damage in lymphocytes. © 2019 The Authors",
publisher = "Churchill Livingstone",
journal = "Medical Hypotheses",
title = "Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy",
volume = "134",
pages = "109419",
doi = "10.1016/j.mehy.2019.109419"
}
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

Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair

Radak, Đorđe J.; Nešković, Mihailo; Otašević, Petar; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Nešković, Mihailo
AU  - Otašević, Petar
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8038
AB  - Abdominal Aortic Aneurysm (AAA) is a degenerative disease of the aortic wall with potentially fatal complications. Open Repair (OR) was considered the gold standard, until the emergence of Endovascular Aneurysm Repair (EVAR), which is less invasive and equally (if not more) effective. As the popularity of endovascular procedures grows, related complications become more evident, with kidney damage being one of them. Although Acute Kidney Injury (AKI) following EVAR is relatively common, its true incidence is still uncertain. Also, there is insufficient data concerning long-term renal outcomes after EVAR, especially with repeated contrast agent exposure. Despite the lack of firm evidence on the effectiveness of individual strategies, it is evident that prevention of AKI following EVAR requires a multifactorial approach. This review focuses on recent findings based on human studies regarding the current evidence of renal impairment after EVAR, its quantification and strategies for its prevention. © 2019 Bentham Science Publishers.
T2  - Current Vascular Pharmacology
T1  - Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair
VL  - 17
IS  - 2
SP  - 133
EP  - 140
DO  - 10.2174/1570161115666171116163203
ER  - 
@article{
author = "Radak, Đorđe J. and Nešković, Mihailo and Otašević, Petar and Isenović, Esma R.",
year = "2019",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8038",
abstract = "Abdominal Aortic Aneurysm (AAA) is a degenerative disease of the aortic wall with potentially fatal complications. Open Repair (OR) was considered the gold standard, until the emergence of Endovascular Aneurysm Repair (EVAR), which is less invasive and equally (if not more) effective. As the popularity of endovascular procedures grows, related complications become more evident, with kidney damage being one of them. Although Acute Kidney Injury (AKI) following EVAR is relatively common, its true incidence is still uncertain. Also, there is insufficient data concerning long-term renal outcomes after EVAR, especially with repeated contrast agent exposure. Despite the lack of firm evidence on the effectiveness of individual strategies, it is evident that prevention of AKI following EVAR requires a multifactorial approach. This review focuses on recent findings based on human studies regarding the current evidence of renal impairment after EVAR, its quantification and strategies for its prevention. © 2019 Bentham Science Publishers.",
journal = "Current Vascular Pharmacology",
title = "Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair",
volume = "17",
number = "2",
pages = "133-140",
doi = "10.2174/1570161115666171116163203"
}
2
3
3

Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair

Radak, Đorđe J.; Nešković, Mihailo; Otašević, Petar; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Nešković, Mihailo
AU  - Otašević, Petar
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8040
AB  - Abdominal Aortic Aneurysm (AAA) is a degenerative disease of the aortic wall with potentially fatal complications. Open Repair (OR) was considered the gold standard, until the emergence of Endovascular Aneurysm Repair (EVAR), which is less invasive and equally (if not more) effective. As the popularity of endovascular procedures grows, related complications become more evident, with kidney damage being one of them. Although Acute Kidney Injury (AKI) following EVAR is relatively common, its true incidence is still uncertain. Also, there is insufficient data concerning long-term renal outcomes after EVAR, especially with repeated contrast agent exposure. Despite the lack of firm evidence on the effectiveness of individual strategies, it is evident that prevention of AKI following EVAR requires a multifactorial approach. This review focuses on recent findings based on human studies regarding the current evidence of renal impairment after EVAR, its quantification and strategies for its prevention. © 2019 Bentham Science Publishers.
T2  - Current Vascular Pharmacology
T1  - Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair
VL  - 17
IS  - 2
SP  - 133
EP  - 140
DO  - 10.2174/1570161115666171116163203
ER  - 
@article{
author = "Radak, Đorđe J. and Nešković, Mihailo and Otašević, Petar and Isenović, Esma R.",
year = "2019",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8040",
abstract = "Abdominal Aortic Aneurysm (AAA) is a degenerative disease of the aortic wall with potentially fatal complications. Open Repair (OR) was considered the gold standard, until the emergence of Endovascular Aneurysm Repair (EVAR), which is less invasive and equally (if not more) effective. As the popularity of endovascular procedures grows, related complications become more evident, with kidney damage being one of them. Although Acute Kidney Injury (AKI) following EVAR is relatively common, its true incidence is still uncertain. Also, there is insufficient data concerning long-term renal outcomes after EVAR, especially with repeated contrast agent exposure. Despite the lack of firm evidence on the effectiveness of individual strategies, it is evident that prevention of AKI following EVAR requires a multifactorial approach. This review focuses on recent findings based on human studies regarding the current evidence of renal impairment after EVAR, its quantification and strategies for its prevention. © 2019 Bentham Science Publishers.",
journal = "Current Vascular Pharmacology",
title = "Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair",
volume = "17",
number = "2",
pages = "133-140",
doi = "10.2174/1570161115666171116163203"
}
2
3
3

Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease

Bajić, Vladan P.; Van Neste, Christophe; Obradović, Milan M.; Zafirović, Sonja; Radak, Đorđe J.; Bajić, Vladimir B.; Essack, Magbubah; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Bajić, Vladan P.
AU  - Van Neste, Christophe
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Radak, Đorđe J.
AU  - Bajić, Vladimir B.
AU  - Essack, Magbubah
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8375
AB  - More people die from cardiovascular diseases (CVD) than from any other cause. Cardiovascular complications are thought to arise from enhanced levels of free radicals causing impaired “redox homeostasis,” which represents the interplay between oxidative stress (OS) and reductive stress (RS). In this review, we compile several experimental research findings that show sustained shifts towards OS will alter the homeostatic redox mechanism to cause cardiovascular complications, as well as findings that show a prolonged antioxidant state or RS can similarly lead to such cardiovascular complications. This experimental evidence is specifically focused on the role of glutathione, the most abundant antioxidant in the heart, in a redox homeostatic mechanism that has been shifted towards OS or RS. This may lead to impairment of cellular signaling mechanisms and elevated pools of proteotoxicity associated with cardiac dysfunction.
T2  - Oxidative Medicine and Cellular Longevity
T1  - Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease
VL  - 2019
SP  - 5028181
DO  - 10.1155/2019/5028181
ER  - 
@article{
author = "Bajić, Vladan P. and Van Neste, Christophe and Obradović, Milan M. and Zafirović, Sonja and Radak, Đorđe J. and Bajić, Vladimir B. and Essack, Magbubah and Isenović, Esma R.",
year = "2019",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8375",
abstract = "More people die from cardiovascular diseases (CVD) than from any other cause. Cardiovascular complications are thought to arise from enhanced levels of free radicals causing impaired “redox homeostasis,” which represents the interplay between oxidative stress (OS) and reductive stress (RS). In this review, we compile several experimental research findings that show sustained shifts towards OS will alter the homeostatic redox mechanism to cause cardiovascular complications, as well as findings that show a prolonged antioxidant state or RS can similarly lead to such cardiovascular complications. This experimental evidence is specifically focused on the role of glutathione, the most abundant antioxidant in the heart, in a redox homeostatic mechanism that has been shifted towards OS or RS. This may lead to impairment of cellular signaling mechanisms and elevated pools of proteotoxicity associated with cardiac dysfunction.",
journal = "Oxidative Medicine and Cellular Longevity",
title = "Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease",
volume = "2019",
pages = "5028181",
doi = "10.1155/2019/5028181"
}
1
14
9
12

Literature-Based Enrichment Insights into Redox Control of Vascular Biology

Essack, Magbubah; Salhi, Adil; Stanimirović, Julijana; Tifratene, Faroug; Bin Raies, Arwa; Hungler, Arnaud; Uludag, Mahmut; Van Neste, Christophe; Trpković, Andreja; Bajić, Vladan P.; Bajić, Vladimir B.; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Essack, Magbubah
AU  - Salhi, Adil
AU  - Stanimirović, Julijana
AU  - Tifratene, Faroug
AU  - Bin Raies, Arwa
AU  - Hungler, Arnaud
AU  - Uludag, Mahmut
AU  - Van Neste, Christophe
AU  - Trpković, Andreja
AU  - Bajić, Vladan P.
AU  - Bajić, Vladimir B.
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8389
AB  - In cellular physiology and signaling, reactive oxygen species (ROS) play one of the most critical roles. ROS overproduction leads to cellular oxidative stress. This may lead to an irrecoverable imbalance of redox (oxidation-reduction reaction) function that deregulates redox homeostasis, which itself could lead to several diseases including neurodegenerative disease, cardiovascular disease, and cancers. In this study, we focus on the redox effects related to vascular systems in mammals. To support research in this domain, we developed an online knowledge base, DES-RedoxVasc, which enables exploration of information contained in the biomedical scientific literature. The DES-RedoxVasc system analyzed 233399 documents consisting of PubMed abstracts and PubMed Central full-text articles related to different aspects of redox biology in vascular systems. It allows researchers to explore enriched concepts from 28 curated thematic dictionaries, as well as literature-derived potential associations of pairs of such enriched concepts, where associations themselves are statistically enriched. For example, the system allows exploration of associations of pathways, diseases, mutations, genes/proteins, miRNAs, long ncRNAs, toxins, drugs, biological processes, molecular functions, etc. that allow for insights about different aspects of redox effects and control of processes related to the vascular system. Moreover, we deliver case studies about some existing or possibly novel knowledge regarding redox of vascular biology demonstrating the usefulness of DES-RedoxVasc. DES-RedoxVasc is the first compiled knowledge base using text mining for the exploration of this topic.
T2  - Oxidative Medicine and Cellular Longevity
T1  - Literature-Based Enrichment Insights into Redox Control of Vascular Biology
VL  - 2019
SP  - 1769437
DO  - 10.1155/2019/1769437
ER  - 
@article{
author = "Essack, Magbubah and Salhi, Adil and Stanimirović, Julijana and Tifratene, Faroug and Bin Raies, Arwa and Hungler, Arnaud and Uludag, Mahmut and Van Neste, Christophe and Trpković, Andreja and Bajić, Vladan P. and Bajić, Vladimir B. and Isenović, Esma R.",
year = "2019",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8389",
abstract = "In cellular physiology and signaling, reactive oxygen species (ROS) play one of the most critical roles. ROS overproduction leads to cellular oxidative stress. This may lead to an irrecoverable imbalance of redox (oxidation-reduction reaction) function that deregulates redox homeostasis, which itself could lead to several diseases including neurodegenerative disease, cardiovascular disease, and cancers. In this study, we focus on the redox effects related to vascular systems in mammals. To support research in this domain, we developed an online knowledge base, DES-RedoxVasc, which enables exploration of information contained in the biomedical scientific literature. The DES-RedoxVasc system analyzed 233399 documents consisting of PubMed abstracts and PubMed Central full-text articles related to different aspects of redox biology in vascular systems. It allows researchers to explore enriched concepts from 28 curated thematic dictionaries, as well as literature-derived potential associations of pairs of such enriched concepts, where associations themselves are statistically enriched. For example, the system allows exploration of associations of pathways, diseases, mutations, genes/proteins, miRNAs, long ncRNAs, toxins, drugs, biological processes, molecular functions, etc. that allow for insights about different aspects of redox effects and control of processes related to the vascular system. Moreover, we deliver case studies about some existing or possibly novel knowledge regarding redox of vascular biology demonstrating the usefulness of DES-RedoxVasc. DES-RedoxVasc is the first compiled knowledge base using text mining for the exploration of this topic.",
journal = "Oxidative Medicine and Cellular Longevity",
title = "Literature-Based Enrichment Insights into Redox Control of Vascular Biology",
volume = "2019",
pages = "1769437",
doi = "10.1155/2019/1769437"
}
2
1
2

HbA1C as a marker of retrograde glycaemic control in diabetes patient with co-existed beta-thalassaemia: A case report and a literature review

Gluvić, Zoran; Obradović, Milan M.; Lačković, Milena; Samardžić, Vladimir S.; Tica Jevtic, Jelena; Essack, Magbubah; Bajić, Vladimir B.; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Gluvić, Zoran
AU  - Obradović, Milan M.
AU  - Lačković, Milena
AU  - Samardžić, Vladimir S.
AU  - Tica Jevtic, Jelena
AU  - Essack, Magbubah
AU  - Bajić, Vladimir B.
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8484
AB  - What is known and objective: The HbA1C marker used in assessing diabetes control quality is not sufficient in diabetes patients with thalassaemia. Case description: A male diabetic patient with thalassaemia was hospitalized due to distal neuropathic pain, right toe trophic ulcer, unacceptable five-point glycaemic profile and recommended HbA1C value. After simultaneously initiated insulin therapy and management of ulcer by hyperbaric oxygen, the patient showed improved glycaemic control and ulcer healing, which led to the patient's discharge. What is new and conclusion: In thalassaemia and haemoglobinopathies, due to discrepancies in the five-point glycaemic profile and HbA1C values, it is necessary to measure HbA1C with a different method or to determine HbA1C and fructosamine simultaneously. © 2019 The Authors. Journal of Clinical Pharmacy and Therapeutics Published by John Wiley & Sons Ltd.
T2  - Journal of Clinical Pharmacy and Therapeutics
T1  - HbA1C as a marker of retrograde glycaemic control in diabetes patient with co-existed beta-thalassaemia: A case report and a literature review
VL  - 45
IS  - 2
SP  - 379
EP  - 383
DO  - 10.1111/jcpt.13073
ER  - 
@article{
author = "Gluvić, Zoran and Obradović, Milan M. and Lačković, Milena and Samardžić, Vladimir S. and Tica Jevtic, Jelena and Essack, Magbubah and Bajić, Vladimir B. and Isenović, Esma R.",
year = "2019",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8484",
abstract = "What is known and objective: The HbA1C marker used in assessing diabetes control quality is not sufficient in diabetes patients with thalassaemia. Case description: A male diabetic patient with thalassaemia was hospitalized due to distal neuropathic pain, right toe trophic ulcer, unacceptable five-point glycaemic profile and recommended HbA1C value. After simultaneously initiated insulin therapy and management of ulcer by hyperbaric oxygen, the patient showed improved glycaemic control and ulcer healing, which led to the patient's discharge. What is new and conclusion: In thalassaemia and haemoglobinopathies, due to discrepancies in the five-point glycaemic profile and HbA1C values, it is necessary to measure HbA1C with a different method or to determine HbA1C and fructosamine simultaneously. © 2019 The Authors. Journal of Clinical Pharmacy and Therapeutics Published by John Wiley & Sons Ltd.",
journal = "Journal of Clinical Pharmacy and Therapeutics",
title = "HbA1C as a marker of retrograde glycaemic control in diabetes patient with co-existed beta-thalassaemia: A case report and a literature review",
volume = "45",
number = "2",
pages = "379-383",
doi = "10.1111/jcpt.13073"
}
1
1
1

Homocysteine and Hyperhomocysteinaemia

Zarić, Božidarka; Obradović, Milan M.; Bajić, Vladan P.; Haidara, Mohamed A.; Jovanović, Miloš; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Zarić, Božidarka
AU  - Obradović, Milan M.
AU  - Bajić, Vladan P.
AU  - Haidara, Mohamed A.
AU  - Jovanović, Miloš
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8485
AB  - Homocysteine (Hcy) is a thiol group containing the amino acid, which naturally occurs in all humans. Hcy is degraded in the body through two metabolic pathways, while a minor part is excreted through kidneys. The chemical reactions that are necessary for degradation of Hcy require the presence of folic acid, vitamins B6 and B12. Consequently, the level of the total Hcy in the serum is influenced by the presence or absence of these vitamins. An elevated level of the Hcy, hyperhomocysteinemia (HHcy) and homocystinuria is connected with occlusive artery disease, especially in the brain, the heart, and the kidney, in addition to venous thrombosis, chronic renal failure, megaloblastic anemia, osteoporosis, depression, Alzheimer's disease, pregnancy problems, and others. Elevated Hcy levels are connected with various pathologies both in adult and child population. Causes of HHcy include genetic mutations and enzyme deficiencies in 5, 10-methylenetetrahydrofolate reductase (MTHFR) methionine synthase (MS), and cystathionine β-synthase (CβS). HHcy can be caused by deficiencies in the folate, vitamin B12 and to a lesser extent, deficiency in B6 vitamin what influences methionine metabolism. Additionally, HHcy can be caused by the rich diet and renal impairment. This review presents literature data from recent research related to Hcy metabolism and the etiology of the Hcy blood level disorder. In addition, we also described various pathological mechanisms induced by hereditary disturbances or nutritional influences and their association with HHcy induced pathology in adults and children and treatment of these metabolic disorders. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
T2  - Current medicinal chemistry
T1  - Homocysteine and Hyperhomocysteinaemia
VL  - 26
IS  - 16
SP  - 2948
EP  - 2961
DO  - 10.2174/0929867325666180313105949
ER  - 
@article{
author = "Zarić, Božidarka and Obradović, Milan M. and Bajić, Vladan P. and Haidara, Mohamed A. and Jovanović, Miloš and Isenović, Esma R.",
year = "2019",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8485",
abstract = "Homocysteine (Hcy) is a thiol group containing the amino acid, which naturally occurs in all humans. Hcy is degraded in the body through two metabolic pathways, while a minor part is excreted through kidneys. The chemical reactions that are necessary for degradation of Hcy require the presence of folic acid, vitamins B6 and B12. Consequently, the level of the total Hcy in the serum is influenced by the presence or absence of these vitamins. An elevated level of the Hcy, hyperhomocysteinemia (HHcy) and homocystinuria is connected with occlusive artery disease, especially in the brain, the heart, and the kidney, in addition to venous thrombosis, chronic renal failure, megaloblastic anemia, osteoporosis, depression, Alzheimer's disease, pregnancy problems, and others. Elevated Hcy levels are connected with various pathologies both in adult and child population. Causes of HHcy include genetic mutations and enzyme deficiencies in 5, 10-methylenetetrahydrofolate reductase (MTHFR) methionine synthase (MS), and cystathionine β-synthase (CβS). HHcy can be caused by deficiencies in the folate, vitamin B12 and to a lesser extent, deficiency in B6 vitamin what influences methionine metabolism. Additionally, HHcy can be caused by the rich diet and renal impairment. This review presents literature data from recent research related to Hcy metabolism and the etiology of the Hcy blood level disorder. In addition, we also described various pathological mechanisms induced by hereditary disturbances or nutritional influences and their association with HHcy induced pathology in adults and children and treatment of these metabolic disorders. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.",
journal = "Current medicinal chemistry",
title = "Homocysteine and Hyperhomocysteinaemia",
volume = "26",
number = "16",
pages = "2948-2961",
doi = "10.2174/0929867325666180313105949"
}
1
22
18
14

Signalni putevi estradiola uključeni u regulaciju ekspresije i aktivnosti inducibilne azot-monoksid-sintaze i natrijum-kalijum adenozintrifosfataze u srcu gojaznih ženki pacova

Jovanović, Aleksandra

(Универзитет у Београду, Биолошки факултет, 2019)

@phdthesis{
author = "Jovanović, Aleksandra",
year = "2019",
url = "http://nardus.mpn.gov.rs/handle/123456789/11023, http://eteze.bg.ac.rs/application/showtheses?thesesId=6735, https://fedorabg.bg.ac.rs/fedora/get/o:19580/bdef:Content/download, https://plus.sr.cobiss.net/opac7/bib/1025214130, http://vinar.vin.bg.ac.rs/handle/123456789/8726",
abstract = "Gojaznost je oboljenje povezano sa nizom patoloških stanja kao što su: rezistencija na insulin (IR), kardiovaskularne bolesti (KVB) i Diabetes Mellitus tipa 2 (DMT2). Povećana ekspresija i aktivnost inducibilne azot-monoksid-sintaze (iNOS; engl. Inducible Nitric Oxide Synthase) u srcu u stanju gojaznosti, moţe dovesti do apoptoze kardiomiocita i hipertrofije srca, dok sa druge strane gojaznost zdruţena sa IR doprinosi smanjenoj aktivnosti Na+/K+-ATPaze, što dovodi do smanjenja kontraktilnosti vaskulature i razvoja sistemske hipertenzije. Endogeni estradiol svojim delovanjem sprečava nastanak IR i hiperglikemije i ostvaruje pozitivne efekte na kardiovaskularni sistem (KVS), ali sinteza i kardioprotektivni uticaj estradiola mogu biti smanjeni usled razvoja gojaznosti.Estradiol ostvaruje kardioprotektivne tako što utiče na smanjenje ekspresije i aktivnosti iNOS, kao i povećanje ekspresije i aktivnosti Na+/K+-ATPaze, posredstvom različitih signalnih molekula i kinaza, kao što su: supstrat receptora za insulin 1 (IRS-1; engl. Insulin Receptor Substrate)/ fosfatidil-inozitol-3-kinaza (PI3K; engl. Phosphatidylinositide 3-Kinase)/ protein kinaza B (Akt; engl. Protein Kinase B), ekstracelularnim signalima regulisane kinaze 1 i 2 (ERK1/2; engl. Extracellular Signal-Regulated Protein Kinases 1 i 2) kao i RhoA (engl. Ras homolog gene family, member A)/ROCK (engl. Rho-associated protein kinase). Pored direktnog efekta na srce, estradiol posredno reguliše i njegovu funkciju tako sto utiče na metabolizam i transport glukoze i SMK, preko transportera glukoze (GLUT; engl. Glucose Transporters) i translokaze masnih kiselina (FAT; CD36 ; engl. Fatty Acid Translocase).Za izradu ove doktorske disertacije je korišćeno 16 adultnih ţenki pacova soja Wistar, podeljenih u dve eksperimentalne grupe. Prva grupa pacova je tokom 10 nedelja hranjena standardnom laboratorijskom hranom za pacove, dok je druga grupa pacova tokom 10 nedelja hranjena standardnom laboratorijskom hranom obogaćenom sa 42% masti (HF reţim ishrane). Nakon 10 nedelja pacovi su ţrtvovani, sakupljena je krv i izolovan je serum, a srca su ekstrahovana i delovi tkiva su korišćeni za izolovanje proteina i RNK. U serumu pacova je odreĎivana koncentracija estradiola, dok su u lizatu srca pacova odreĎivane koncentracije L-Arginina (L-Arg), NO i slobodnih masnih kiselina (SMK). Metodom qRT-PCR odreĎivan je nivo iRNK iNOS u srcu pacova..., Obesity is associated with several pathological conditions such as: insulin resistance (IR), cardiovascular disease (CVD) and Diabetes Mellitus type 2 (DMT2). Obesity related inducible nitric oxide synthase (iNOS) overexpression could lead to cardiac hypertrophy, while on the other hand obesity induced IR contributes to the reduced Na+/K+-ATPase activity, leading to vascular contractility impairment and development of systemic hypertension. Endogenous estradiol prevents IR and hyperglycaemia and has protective effects on the cardiovascular system (CVS), but the synthesis and cardioprotective effect of estradiol can be reduced due to the development of obesity. Estradiol exerts cardioprotective effects by reducing the expression and activity of iNOS, as well as by increasing the expression of Na+/K+-ATPase activity by regulating the activity of signaling molecules and kinases, such as: insulin receptor substrate 1 (IRS-1)/phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt, PKB), extracellular signal regulated kinase 1 and 2 (ERK1/2) as well as RhoA (Ras homolog gene family, member A)/ROCK (Rho-associated protein kinase). Additionally, estradiol indirectly regulates CVS function by influencing the metabolism and transport of glucose and free fatty acids (FFA), through glucose transporter (GLUT) and FAT; CD36 (Fatty Acid Translocase). In this doctoral dissertation 16 adult female Wistar rats were used and divided into two experimental groups. The first group of rats was fed a standard chow for laboratory rats for 10 weeks, while the second group of rats was fed a standard chow for laboratory rats enriched with 42% fat (HF diet) for 10 weeks. After 10 weeks, the rats were sacrificed, blood was collected and the serum isolated, the hearts were collected, and its tissue fragments were used to isolate proteins and RNA. The concentration of estradiol was measured in serum, while concentrations of L-Arginine (L-Arg), NO and free fatty acids (FFA) were measured in the heart lysates. qRT-PCR method was used to measure the level of iNOS mRNA in rats’ hearts. Na+/K+-ATPase was measured in plasma membranes of rats’ hearts. Western blot was used to measure the level of the following proteins: iNOS, NFkB-p50, ERα, p85 and p110 subunits of PI3K, NDRG2, RhoA, ROCK1 and ROCK2 in heart lysates. The level of phosphorylation and expression of Akt and ERK1/2 kinases, as well as the IRS-1/PI3K associations, were determined in heart lysates...",
publisher = "Универзитет у Београду, Биолошки факултет",
journal = "Универзитет у Београду",
title = "Signalni putevi estradiola uključeni u regulaciju ekspresije i aktivnosti inducibilne azot-monoksid-sintaze i natrijum-kalijum adenozintrifosfataze u srcu gojaznih ženki pacova"
}

Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy

Obradović, Milan M.; Bogdanović, Nikola; Stanimirović, Julijana; Unić-Stojanović, Dragana R.; Radak, Đorđe J.; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Bogdanović, Nikola
AU  - Stanimirović, Julijana
AU  - Unić-Stojanović, Dragana R.
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0306987718308302
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7930
AB  - Sudden occlusion of an artery caused by a thrombus or emboli is the most frequent cause of acute brain ischemia (ABI). Carotid endarterectomy (CEA) represents the gold standard for preventing strokes of carotid origin. However, neuronal damage caused by ischemia and/or reperfusion may contribute to a poor clinical outcome after CEA. In response to shear stress caused by hypoxic-ischemic conditions in patients undergoing CEA, stimulation of the hypothalamic-pituitaryadrenal axis leads to biological responses known as hypermetabolic stress, characterized by hemodynamic, metabolic, inflammatory and immunological changes. These changes maintain homeostasis and assist recovery, but an unregulated inflammatory response could lead to further tissue damage and death of neurons. Nitric oxide (NO) is an important signaling molecule involved in several physiological and pathological processes, including ABI. However, an excess of NO could have detrimental effects. We hypothesized that the hypoxic-ischemic state induced by carotid clamping leads to overexpression of inducible NO synthase and that uncontrolled production of NO could adversely affect outcome after CEA. © 2018 Elsevier Ltd
T2  - Medical Hypotheses
T1  - Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy
VL  - 122
SP  - 16
EP  - 18
DO  - 10.1016/j.mehy.2018.10.011
ER  - 
@article{
author = "Obradović, Milan M. and Bogdanović, Nikola and Stanimirović, Julijana and Unić-Stojanović, Dragana R. and Radak, Đorđe J. and Isenović, Esma R.",
year = "2019",
url = "https://linkinghub.elsevier.com/retrieve/pii/S0306987718308302, http://vinar.vin.bg.ac.rs/handle/123456789/7930",
abstract = "Sudden occlusion of an artery caused by a thrombus or emboli is the most frequent cause of acute brain ischemia (ABI). Carotid endarterectomy (CEA) represents the gold standard for preventing strokes of carotid origin. However, neuronal damage caused by ischemia and/or reperfusion may contribute to a poor clinical outcome after CEA. In response to shear stress caused by hypoxic-ischemic conditions in patients undergoing CEA, stimulation of the hypothalamic-pituitaryadrenal axis leads to biological responses known as hypermetabolic stress, characterized by hemodynamic, metabolic, inflammatory and immunological changes. These changes maintain homeostasis and assist recovery, but an unregulated inflammatory response could lead to further tissue damage and death of neurons. Nitric oxide (NO) is an important signaling molecule involved in several physiological and pathological processes, including ABI. However, an excess of NO could have detrimental effects. We hypothesized that the hypoxic-ischemic state induced by carotid clamping leads to overexpression of inducible NO synthase and that uncontrolled production of NO could adversely affect outcome after CEA. © 2018 Elsevier Ltd",
journal = "Medical Hypotheses",
title = "Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy",
volume = "122",
pages = "16-18",
doi = "10.1016/j.mehy.2018.10.011"
}
2
3
1
1

The Significance of Pain in Chronic Venous Disease and its Medical Treatment

Radak, Đorđe J.; Atanasijević, Igor; Nešković, Mihailo; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Atanasijević, Igor
AU  - Nešković, Mihailo
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://www.eurekaselect.com/159661/article
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8098
AB  - Chronic venous disease (CVeD) is a highly prevalent condition in the general population, and it has a significant impact on quality of life. While it is usually manifested by obvious signs, such as varicose veins and venous ulcers, other symptoms of the disease are less specific. Among the other symptoms, which include heaviness, swelling, muscle cramps and restless legs, pain is the symptom that most frequently compels CVeD patients to seek medical aid. However, there is a substantial discrepancy between pain severity and clinically detectable signs of CVeD, questioned by several opposing studies. Further evaluation is needed to clarify this subject, and to analyse whether pain development predicts objective CVeD progression. General management of CVeD starts with advising lifestyle changes, such as lowering body mass index and treating comorbidities. However, the mainstay of treatment is compression therapy, with the additional use of pharmacological substances. Venoactive drugs proved to be the drugs of choice for symptom alleviation and slowing the progression of CVeD, with micronized purified flavonoid fraction being the most effective one. Interventional therapy is reserved for advanced stages of the disease.
T2  - Current Vascular Pharmacology
T1  - The Significance of Pain in Chronic Venous Disease and its Medical Treatment
VL  - 17
IS  - 3
SP  - 291
EP  - 297
DO  - 10.2174/1570161116666180209111826
ER  - 
@article{
author = "Radak, Đorđe J. and Atanasijević, Igor and Nešković, Mihailo and Isenović, Esma R.",
year = "2019",
url = "http://www.eurekaselect.com/159661/article, http://vinar.vin.bg.ac.rs/handle/123456789/8098",
abstract = "Chronic venous disease (CVeD) is a highly prevalent condition in the general population, and it has a significant impact on quality of life. While it is usually manifested by obvious signs, such as varicose veins and venous ulcers, other symptoms of the disease are less specific. Among the other symptoms, which include heaviness, swelling, muscle cramps and restless legs, pain is the symptom that most frequently compels CVeD patients to seek medical aid. However, there is a substantial discrepancy between pain severity and clinically detectable signs of CVeD, questioned by several opposing studies. Further evaluation is needed to clarify this subject, and to analyse whether pain development predicts objective CVeD progression. General management of CVeD starts with advising lifestyle changes, such as lowering body mass index and treating comorbidities. However, the mainstay of treatment is compression therapy, with the additional use of pharmacological substances. Venoactive drugs proved to be the drugs of choice for symptom alleviation and slowing the progression of CVeD, with micronized purified flavonoid fraction being the most effective one. Interventional therapy is reserved for advanced stages of the disease.",
journal = "Current Vascular Pharmacology",
title = "The Significance of Pain in Chronic Venous Disease and its Medical Treatment",
volume = "17",
number = "3",
pages = "291-297",
doi = "10.2174/1570161116666180209111826"
}
1
1
1

Effects of IGF-1 on the cardiovascular system

Obradović, Milan M.; Zafirović, Sonja; Soskić, Sanja S.; Stanimirović, Julijana; Trpković, Andreja; Jevremović, Danimir P.; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Soskić, Sanja S.
AU  - Stanimirović, Julijana
AU  - Trpković, Andreja
AU  - Jevremović, Danimir P.
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8483
AB  - Cardiovascular (CV) diseases are the most common health problems worldwide, with a permanent increase in incidence. Growing evidence underlines that insulin-like growth factor 1 (IGF-1) is a very important hormone responsible for normal CV system physiology. IGF-1 is an anabolic growth hormone, responsible for cell growth, differentiation, proliferation, and survival. Despite systemic effects, IGF-1 exerts a wide array of influences in the CV system affecting metabolic homeostasis, vasorelaxation, cardiac contractility and hypertrophy, autophagy, apoptosis, and antioxidative processes. The vasodilatory effect of IGF-1, is achieved through the regulation of the activity of endothelial nitric oxide synthase (eNOS) and, at least partly, through enhancing inducible NOS (iNOS) activity. Also, IGF-1 stimulates vascular relaxation through regulation of sodium/potassium-adenosine-triphosphatase. Numerous animal studies provided evidence of diverse influences of IGF-1 in the CV system such as vasorelaxation, anti-apoptotic and prosurvival effects. Human studies indicate that low serum levels of free or total IGF-1 contribute to an increased risk of CV and cerebrovascular disease. Large human trials aiming at finding clinical efficacy and outcome of IGF-1-related therapy are of great interest. We look forward to the development of new IGF 1 therapies with minor side effects. In this review, we discuss the latest literature data regarding the function of IGF-1 in the CV system in the physiological and pathophysiological conditions. © 2019 Bentham Science Publishers.
T2  - Current Pharmaceutical Design
T1  - Effects of IGF-1 on the cardiovascular system
VL  - 25
IS  - 35
SP  - 3715
EP  - 3725
DO  - 10.2174/1381612825666191106091507
ER  - 
@article{
author = "Obradović, Milan M. and Zafirović, Sonja and Soskić, Sanja S. and Stanimirović, Julijana and Trpković, Andreja and Jevremović, Danimir P. and Isenović, Esma R.",
year = "2019",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8483",
abstract = "Cardiovascular (CV) diseases are the most common health problems worldwide, with a permanent increase in incidence. Growing evidence underlines that insulin-like growth factor 1 (IGF-1) is a very important hormone responsible for normal CV system physiology. IGF-1 is an anabolic growth hormone, responsible for cell growth, differentiation, proliferation, and survival. Despite systemic effects, IGF-1 exerts a wide array of influences in the CV system affecting metabolic homeostasis, vasorelaxation, cardiac contractility and hypertrophy, autophagy, apoptosis, and antioxidative processes. The vasodilatory effect of IGF-1, is achieved through the regulation of the activity of endothelial nitric oxide synthase (eNOS) and, at least partly, through enhancing inducible NOS (iNOS) activity. Also, IGF-1 stimulates vascular relaxation through regulation of sodium/potassium-adenosine-triphosphatase. Numerous animal studies provided evidence of diverse influences of IGF-1 in the CV system such as vasorelaxation, anti-apoptotic and prosurvival effects. Human studies indicate that low serum levels of free or total IGF-1 contribute to an increased risk of CV and cerebrovascular disease. Large human trials aiming at finding clinical efficacy and outcome of IGF-1-related therapy are of great interest. We look forward to the development of new IGF 1 therapies with minor side effects. In this review, we discuss the latest literature data regarding the function of IGF-1 in the CV system in the physiological and pathophysiological conditions. © 2019 Bentham Science Publishers.",
journal = "Current Pharmaceutical Design",
title = "Effects of IGF-1 on the cardiovascular system",
volume = "25",
number = "35",
pages = "3715-3725",
doi = "10.2174/1381612825666191106091507"
}
2
3
3

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

Regulation of hepatic Na+/K+-ATPase in obese female and male rats: involvement of ERK1/2, AMPK, and Rho/ROCK

(2018)

TY  - JOUR
PY  - 2018
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7581
AB  - In this study, we assessed whether the disturbed regulation of sodium/potassium-adenosine-triphosphatase (Na+/K+-ATPase) occurs as a consequence of obesity-induced IR in sex-specific manner. We also assessed whether alterations of IRS/PI3K/Akt, ERK1/2, AMPK alpha, and RhoA/ROCK signaling cascades have an important role in this pathology. Female and male Wistar rats (150-200 g, 8 weeks old) were fed a standard laboratory diet or a high-fat (HF) diet (42% fat) for 10 weeks. The activity of hepatic Na+/K+-ATPase and Rho, and the association of IRS-1/p85 were assessed in liver. Furthermore, the protein level of alpha(1) Na+/K+-ATPase in plasma membrane fractions, and protein levels of IRS-1, PI3K-p85, -p110, RhoA, ROCK1, ROCK2, ERK1/2, AMPK alpha, ER alpha, and ER beta in liver lysates were assessed. The expression of hepatic alpha(1) Na+/K+-ATPase mRNA was also analyzed by qRT-PCR. The results show that HF-fed female rats exhibited an increase in hepatic ERK1/2 (p < 0.05) and AMPK alpha (p < 0.05) phosphorylation levels, unchanged level of Na+/K+-ATPase alpha(1) mRNA, decreased level of Na+/K+-ATPase activity (p < 0.05), and decreased alpha(1) Na+/K+-ATPase protein expression (p < 0.01). In liver of HF-fed male rats, results show decreased levels of Na+/K+-ATPase activity (p < 0.01), both protein and mRNA of alpha(1) subunit (p < 0.05), but significant increase in Rho activity (p < 0.05). Our results indicate significant sex differences in alpha(1) Na+/K+-ATPase mRNA expression and activation of ERK1/2, AMPK alpha, and Rho in the liver. Exploring the sex-specific factors and pathways that promote obesity-related diseases may lead to a better understanding of pathogenesis and discovering new therapeutic targets.
T2  - Molecular and Cellular Biochemistry
T1  - Regulation of hepatic Na+/K+-ATPase in obese female and male rats: involvement of ERK1/2, AMPK, and Rho/ROCK
VL  - 440
SP  - 77
EP  - 88
DO  - 10.1007/s11010-017-3157-z
ER  - 
@article{
year = "2018",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/7581",
abstract = "In this study, we assessed whether the disturbed regulation of sodium/potassium-adenosine-triphosphatase (Na+/K+-ATPase) occurs as a consequence of obesity-induced IR in sex-specific manner. We also assessed whether alterations of IRS/PI3K/Akt, ERK1/2, AMPK alpha, and RhoA/ROCK signaling cascades have an important role in this pathology. Female and male Wistar rats (150-200 g, 8 weeks old) were fed a standard laboratory diet or a high-fat (HF) diet (42% fat) for 10 weeks. The activity of hepatic Na+/K+-ATPase and Rho, and the association of IRS-1/p85 were assessed in liver. Furthermore, the protein level of alpha(1) Na+/K+-ATPase in plasma membrane fractions, and protein levels of IRS-1, PI3K-p85, -p110, RhoA, ROCK1, ROCK2, ERK1/2, AMPK alpha, ER alpha, and ER beta in liver lysates were assessed. The expression of hepatic alpha(1) Na+/K+-ATPase mRNA was also analyzed by qRT-PCR. The results show that HF-fed female rats exhibited an increase in hepatic ERK1/2 (p < 0.05) and AMPK alpha (p < 0.05) phosphorylation levels, unchanged level of Na+/K+-ATPase alpha(1) mRNA, decreased level of Na+/K+-ATPase activity (p < 0.05), and decreased alpha(1) Na+/K+-ATPase protein expression (p < 0.01). In liver of HF-fed male rats, results show decreased levels of Na+/K+-ATPase activity (p < 0.01), both protein and mRNA of alpha(1) subunit (p < 0.05), but significant increase in Rho activity (p < 0.05). Our results indicate significant sex differences in alpha(1) Na+/K+-ATPase mRNA expression and activation of ERK1/2, AMPK alpha, and Rho in the liver. Exploring the sex-specific factors and pathways that promote obesity-related diseases may lead to a better understanding of pathogenesis and discovering new therapeutic targets.",
journal = "Molecular and Cellular Biochemistry",
title = "Regulation of hepatic Na+/K+-ATPase in obese female and male rats: involvement of ERK1/2, AMPK, and Rho/ROCK",
volume = "440",
pages = "77-88",
doi = "10.1007/s11010-017-3157-z"
}
7
5
3

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"
}
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Efekat estradiola na regulaciju endotelne i inducibilne azot-monoksid-sintaze u srcu gojaznih pacova

Zafirović, Sonja

(Универзитет у Београду, Биолошки факултет, 2018)

@phdthesis{
author = "Zafirović, Sonja",
year = "2018",
url = "http://eteze.bg.ac.rs/application/showtheses?thesesId=6031, https://fedorabg.bg.ac.rs/fedora/get/o:18344/bdef:Content/download, http://www.vbs.rs/scripts/cobiss?command=DISPLAY&base=99999&rid=50433295&fmt=11&lani=sc, http://nardus.mpn.gov.rs/123456789/9980, http://vinar.vin.bg.ac.rs/handle/123456789/7955",
abstract = "Estradiol ostvaruje pozitivan efekat na kardiovaskularni sistem (KVS), sprečavanjem nastanka ateroskleroze i endotelne i/ili vaskularne disfunkcije, a deluje i direktno na srce smanjujući njegovu hipertrofiju. Estradiol ostvaruje pozitivne efekte u KVS regulacijom azot-monoksid (NO)-sintaza (NOS), endotelne (eNOS) i inducibilne (iNOS) forme, koje su odgovorne za sintezu NO, aktivacijom sloţene mreţe unutarćelijskih signalnih puteva, u koje su uključeni signalni molekuli supstrat receptora za insulin 1 (IRS-1), fosfatidil-inozitol-3-kinaza (PI3K) i protein kinaza B (Akt). Estradiol utiče na signalnu transdukciju angiotenzina II (Ang II), delujući na ekspresiju receptora za Ang II tipa 1 (AT1R) i tipa 2 (AT2R), kao i na nivo RhoA proteina. Estradiol utiče i na transport energetskih supstrata regulišući translokazu masnih kiselina (CD36) i transportere za glukozu tipa 1 (GLUT1) i tipa 4 (GLUT4). Kontrolni i gojazni muţjaci pacova soja Wistar tretirani su estradiolom (40μg/kg) ili 1% etanolom 24 sata pre ţrtvovanja. Spektrofotometrijskim metodama određivane su koncentracije NO u plazmi i koncentracije L-Arginina (L-Arg), NO i slobodnih masnih kiselina (SMK) u lizatu srca. Western blot metodom određivani su nivoi proteina eNOS, iNOS, NF-κB-p65, pIRS-1/IRS-1, p85 i p110 subjedinice PI3K, pAkt/Akt, RhoA, AT1R, AT2R, GLUT1, GLUT4 i CD36 proteina, kao i asocijacija IRS-1 sa p85-PI3K proteinom u srcu pacova, dok je imunohistohemijskom metodom određivana ekspresija i lokalizacija eNOS i iNOS. Metodom qRT-PCR određivan je nivo iRNK za eNOS i iNOS u srcu pacova. Rezultati su analizirani korišćenjem Studentovog t-testa. Rezultati prikazani u ovoj doktorskoj disertaciji pokazuju da tretman estradiolom kod kontrolnih pacova povećava nivo p85 subjedinice PI3K ifosforilaciju Akt na Thr308, dok smanjuje ekspresiju gena za iNOS..., Estradiol has a positive effect on the cardiovascular system (CVS) by preventing the development of atherosclerosis and endothelial and/or vascular dysfunction. Estradiol exerts many of its effects on the CVS by regulation of nitric oxide synthase (NOS), endothelial (eNOS) and inducible (iNOS) forms that are responsible for the synthesis of nitric oxide (NO), through activation of the complex network of intercellular signal pathways that include signaling molecules: insulin receptor substrate 1 (IRS-1), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt.) Estradiol also affects the signal transduction of angiotensin II (Ang II) by affecting the expression of Ang II receptors: type 1 (AT1R) and type 2 (AT2R), as well as the level of RhoA protein. Finally, estradiol indirectly regulates the transport of energy substrates in heart, by regulating transporters of free fatty acids (FFA) and glucose, CD36 and glucose transporters type 1 (GLUT1) and type 4 (GLUT4).Control and obese male Wistar rats were treated with one dose of estradiol (40 μg/kg) or with the same amount of 1% ethanol in saline 24 hours before sacrificed. The concentration of NO was measured in the plasma and in lysates, while the concentrations of L-Arginine and FFA were determined in the lysates of the rats‘ hearts. The Western blot method was used to determine the level of eNOS, iNOS, NF-kB p65, IRS-1, p85 and p110 subunits of PI3K, Akt, AT1R, AT2R, RhoA, CD36, GLUT1 and GLUT4 in the rats‘ heart, as well as association of IRS-1 with p85 subunit of PI3K. Immunohistochemical analysis was used for localization and expression of eNOS and iNOS proteins in heart. qRT-PCR was used to determen the level of iRNA of eNOS and iNOS in rats‘ heart. Results were analyzed using Student‘s t test...",
publisher = "Универзитет у Београду, Биолошки факултет",
journal = "Универзитет у Београду",
title = "Efekat estradiola na regulaciju endotelne i inducibilne azot-monoksid-sintaze u srcu gojaznih pacova"
}

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"
}
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