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Obradović, Milan M.

Link to this page

Authority KeyName Variants
orcid::0000-0002-4769-2652
  • Obradović, Milan M. (53)
Projects
Hormonal regulation of expression and activity of the nitric oxide synthase and sodium-potassium pump in experimental models of insulin resistance, diabetes and cardiovascular disorders Carotid disease in Serbia - pathologic dynamics, prevention, diagnostics and inovative therapeutic methods
Cell Cycle Aberrations and the Impact of Oxidative Stress in Neurodegenerative Processes and Malignant Transformation of the Cell An integral study to identify the regional genetic and environmental risk factors for the common noncommunicable diseases in the human population of Serbia - INGEMA_S
KAUST Office of Sponsored Research (OSR) [FCC/1/1976-17-01] KAUST Base Research Fund [BAS/1/1606-01-01]
CNRS, University Pierre and Marie Curie, Pavle Savic [337-00-359/2005-01/16], Republic of France, Ministry of Foreign Affairs CNRS, University Pierre and Marie Curie, Republic of France, Ministry of Foreign Affairs, [337-00-359/2005-01/16]
COST Action [CA15132, ‘hCOMET’] The study of physicochemical and biochemical processes in living environment that have impacts on pollution and the investigation of possibilities for minimizing the consequences
Application of the EIIP/ISM bioinformatics platform in discovery of novel therapeutic targets and potential therapeutic molecules Effects of metabolic and nonmetabolic stressors on the expression and action of neuroendocrine regulators of energy homeostasis
Molecular determinants for tumor marker design Effects of modulation of biohumoral, inflammatory and metabolic response in acute ST-segment elevation myocardial infarction on survival and left ventricular function
KAUST [4129] KAUST Base Research Fund [BAS/1/1606‐01‐01]
KAUST Base Research Funds [BAS/1/1059-01-01] KAUST Base Research Funds [BAS/1/1606-01-01]
KAUST grant [OSR#4129] KAUST grant OSR#4 129
KAUST Office of Sponsored Research (OSR) Awards [FCC/1/1976-24-01] KAUST Office of Sponsored Research (OSR) [FCC/1/1976‐17‐01]
KAUST Office of Sponsored Research (OSR) [FCC/1/1976‐24‐01] KAUST [OSR#4129]
King Abdullah University of Science and Technology (KAUST) Base Research Fund [BAS/1/1606-01-01]

Author's Bibliography

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

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

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

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
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
18

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

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

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

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"
}
1
3
2
3

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

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

(2018)

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

The role of eNOS and iNOS in pathophysiological conditions

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

(Nova Science Publishers, 2018)

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

Relationship between Vitamin D and Metalloproteinases (MMPs) in Acute Myocardial Infarction (AMI) (Editorial)

Perović, Milan; Obradović, Milan M.; Resanović, Ivana; Isenović, Esma R.

(2018)

TY  - JOUR
AU  - Perović, Milan
AU  - Obradović, Milan M.
AU  - Resanović, Ivana
AU  - Isenović, Esma R.
PY  - 2018
UR  - http://www.eurekaselect.com/156167/article
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7749
T2  - Current Vascular Pharmacology
T1  - Relationship between Vitamin D and Metalloproteinases (MMPs) in Acute Myocardial Infarction (AMI) (Editorial)
VL  - 16
IS  - 4
SP  - 361
EP  - 362
DO  - 10.2174/1570161115999171004111230
ER  - 
@article{
author = "Perović, Milan and Obradović, Milan M. and Resanović, Ivana and Isenović, Esma R.",
year = "2018",
url = "http://www.eurekaselect.com/156167/article, http://vinar.vin.bg.ac.rs/handle/123456789/7749",
journal = "Current Vascular Pharmacology",
title = "Relationship between Vitamin D and Metalloproteinases (MMPs) in Acute Myocardial Infarction (AMI) (Editorial)",
volume = "16",
number = "4",
pages = "361-362",
doi = "10.2174/1570161115999171004111230"
}
1

PCSK9 and Hypercholesterolemia: Therapeutic Approach

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

(2018)

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

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

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

(2018)

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

IGF-1 ameliorates detrimental effects of obesity in rat heart by promoting akt and FOXO1

Stanimirović, Julijana; Panić, Anastasija; Obradović, Milan M.; Zafirović, Sonja; Isenović, Esma R.

(2018)

TY  - CONF
AU  - Stanimirović, Julijana
AU  - Panić, Anastasija
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Isenović, Esma R.
PY  - 2018
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0021915018307147
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7948
C3  - Atherosclerosis
T1  - IGF-1 ameliorates detrimental effects of obesity in rat heart by promoting akt and FOXO1
VL  - 275
SP  - e137
DO  - 10.1016/j.atherosclerosis.2018.06.402
ER  - 
@conference{
author = "Stanimirović, Julijana and Panić, Anastasija and Obradović, Milan M. and Zafirović, Sonja and Isenović, Esma R.",
year = "2018",
url = "https://linkinghub.elsevier.com/retrieve/pii/S0021915018307147, http://vinar.vin.bg.ac.rs/handle/123456789/7948",
journal = "Atherosclerosis",
title = "IGF-1 ameliorates detrimental effects of obesity in rat heart by promoting akt and FOXO1",
volume = "275",
pages = "e137",
doi = "10.1016/j.atherosclerosis.2018.06.402"
}

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

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

(2018)

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

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

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

(2017)

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

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

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

(2017)

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

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

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

(2017)

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

MicroRNA in breast cancer: The association with BRCA1/2

Petrović, Nina; Davidović, Radoslav S.; Bajić, Vladan P.; Obradović, Milan M.; Isenović, Esma R.

(2017)

@article{
author = "Petrović, Nina and Davidović, Radoslav S. and Bajić, Vladan P. and Obradović, Milan M. and Isenović, Esma R.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1614",
abstract = "Breast cancer (BC) is a heterogeneous disease in an urgent need for developing novel research, classification, and therapy approaches. Breast cancer 1 (BRCA1) and breast cancer 2 (BRCA2) proteins are well described tumor suppressors with great potential to be the subjects of different therapies. MicroRNAs (miRNAs) are genetic elements that might be used to solve the complex BC puzzle. BRCA1 was described to be the target of up to 100 miRNAs. BRCA1 may directly repress miR-155 activity. In addition, miR-15/107/182-mediated downregulation of BRCA1 interrupt DNA repair and may change the course of BC therapy. miR-146a and miR-146-5p silencing BRCA1 may trigger formation of triple-negative and basal-like sporadic BC cases. miR-182 might effect the therapy outcome. miR-21 targeted therapy might be useful for the treatment of BRCA2 mutation carriers. miR-342 overexpression and the absence of functional BRCA1 gene might cause synthetic lethality, which might be used as a base for future therapies. The present review discusses the latest data from studies that focus on the complex network of miRNAs and BRCA1/2 related BCs, which might be important for improving the therapy within the patients with triple-negative BC (TNBC) and basal-like BC, and for understanding the formation of TNBC.",
journal = "Cancer Biomarkers",
title = "MicroRNA in breast cancer: The association with BRCA1/2",
volume = "19",
number = "2",
pages = "119-128",
doi = "10.3233/CBM-60319"
}
21