Sort By
Publication Year
Deposit Date
Title
Type
Access
Publication Year
2020 (2)
2019 (3)
2018 (4)
2017 (2)
2016 (1)
2012 (2)
2011 (2)
2009 (1)
2008 (1)
2007 (2)
Type
Version
M-Rank
M13 (1)
M21 (3)
M21~ (1)
M21a (1)
M22 (1)
M22~ (1)
M23 (5)

Zarić, Božidarka

Link to this page

Authority KeyName Variants
orcid::0000-0003-4244-3283
  • Zarić, Božidarka (20)
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 The study of physicochemical and biochemical processes in living environment that have impacts on pollution and the investigation of possibilities for minimizing the consequences
Carotid disease in Serbia - pathologic dynamics, prevention, diagnostics and inovative therapeutic methods Studies of enzyme interactions with toxic and pharmacologically active molecules
Beneficentia Stiftung (Vaduz), ITT (Istituto Toscano Tumori), Fondazione Cassa Risparmio Firenze (CRF), AIRC [IG-16049], AIRC-FIRC (Fondazione Italiana per la Ricerca sul Cancro) [18044] CNRS, University Pierre and Marie Curie, Ministry of Science, Republic of Serbia [143030B], Pavle Savic [337-00-359/2005-01/16], Republic of France, Ministry of Foreign Affairs
Application of the EIIP/ISM bioinformatics platform in discovery of novel therapeutic targets and potential therapeutic molecules Cell Cycle Aberrations and the Impact of Oxidative Stress in Neurodegenerative Processes and Malignant Transformation of the Cell
Structural characterisation of the insulin-like growth factor (IGF) binding proteins and IGF receptors, their interactions with other physiological molecules and alterations in metabolic disorders Biological effects, nutritional intake and status of folate and polysaturate fatty acid (PUFA): improvement of nutrition in Serbia
NIGMS NIH HHS [GM72481]

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

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

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

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

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

Interaction of Au(iii) and Pt(ii) complexes with Na/K-ATPase: experimental and theoretical study of reaction stoichiometry and binding sites

Vujačić Nikezić, Ana V.; Janjić, Goran V.; Bondžić, Aleksandra; Zarić, Božidarka; Vasić Anićijević, Dragana D.; Momić, Tatjana; Vasić, Vesna M.

(2018)

TY  - JOUR
AU  - Vujačić Nikezić, Ana V.
AU  - Janjić, Goran V.
AU  - Bondžić, Aleksandra
AU  - Zarić, Božidarka
AU  - Vasić Anićijević, Dragana D.
AU  - Momić, Tatjana
AU  - Vasić, Vesna M.
PY  - 2018
UR  - http://xlink.rsc.org/?DOI=C8MT00111A
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7812
AB  - The present paper deals with investigation of the interaction between selected simple structure Au(iii) ([AuCl4]-, [AuCl2(dmso)2]+, [AuCl2(bipy)]+) and Pt(ii) ([PtCl2(dmso)2]) complexes with Na/K-ATPase as the target enzyme, using an experimental and theoretical approach. Reaction stoichiometries and binding constants for these enzyme/complex systems were determined, while kinetic measurements were used in order to reveal the type of inhibition. Based on the results obtained by quantum mechanical calculations (electrostatic surface potential (ESP), volume and surface of the complexes) the nature of the investigated complexes was characterized. By using the solvent accessible surface area (SASA) applied on specific inhibitory sites (ion channel and intracellular domains) the nature of these sites was described. Docking studies were used to determine the theoretical probability of the non-covalent metal binding site positions. Inhibition studies implied that all the investigated complexes decreased the activity of the enzyme while the kinetic analysis indicated an uncompetitive mode of inhibition for the selected complexes. Docking results suggested that the main inhibitory site of all these complexes is located in the ion translocation pathway on the extracellular side in the E2P enzyme conformation, similar to the case of cardiac glycosides, specific Na/K-ATPase inhibitors. Also, based on our knowledge, the hydrolyzed forms of [AuCl4]- and [PtCl2(dmso)2] complexes were investigated for the first time by theoretical calculations in this paper. Thereby, a new inhibitory site situated between the M2 and M4 helices was revealed. Binding in this site induces conformational changes in the enzyme domains and perturbs the E1-E2P conformational equilibrium, causing enzyme inhibition.
T2  - Metallomics
T1  - Interaction of Au(iii) and Pt(ii) complexes with Na/K-ATPase: experimental and theoretical study of reaction stoichiometry and binding sites
VL  - 10
IS  - 7
SP  - 1003
EP  - 1015
DO  - 10.1039/C8MT00111A
ER  - 
@article{
author = "Vujačić Nikezić, Ana V. and Janjić, Goran V. and Bondžić, Aleksandra and Zarić, Božidarka and Vasić Anićijević, Dragana D. and Momić, Tatjana and Vasić, Vesna M.",
year = "2018",
url = "http://xlink.rsc.org/?DOI=C8MT00111A, http://vinar.vin.bg.ac.rs/handle/123456789/7812",
abstract = "The present paper deals with investigation of the interaction between selected simple structure Au(iii) ([AuCl4]-, [AuCl2(dmso)2]+, [AuCl2(bipy)]+) and Pt(ii) ([PtCl2(dmso)2]) complexes with Na/K-ATPase as the target enzyme, using an experimental and theoretical approach. Reaction stoichiometries and binding constants for these enzyme/complex systems were determined, while kinetic measurements were used in order to reveal the type of inhibition. Based on the results obtained by quantum mechanical calculations (electrostatic surface potential (ESP), volume and surface of the complexes) the nature of the investigated complexes was characterized. By using the solvent accessible surface area (SASA) applied on specific inhibitory sites (ion channel and intracellular domains) the nature of these sites was described. Docking studies were used to determine the theoretical probability of the non-covalent metal binding site positions. Inhibition studies implied that all the investigated complexes decreased the activity of the enzyme while the kinetic analysis indicated an uncompetitive mode of inhibition for the selected complexes. Docking results suggested that the main inhibitory site of all these complexes is located in the ion translocation pathway on the extracellular side in the E2P enzyme conformation, similar to the case of cardiac glycosides, specific Na/K-ATPase inhibitors. Also, based on our knowledge, the hydrolyzed forms of [AuCl4]- and [PtCl2(dmso)2] complexes were investigated for the first time by theoretical calculations in this paper. Thereby, a new inhibitory site situated between the M2 and M4 helices was revealed. Binding in this site induces conformational changes in the enzyme domains and perturbs the E1-E2P conformational equilibrium, causing enzyme inhibition.",
journal = "Metallomics",
title = "Interaction of Au(iii) and Pt(ii) complexes with Na/K-ATPase: experimental and theoretical study of reaction stoichiometry and binding sites",
volume = "10",
number = "7",
pages = "1003-1015",
doi = "10.1039/C8MT00111A"
}
1
1
1

Genetic Markers for Coronary Artery Disease

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

(2018)

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

The role of eNOS and iNOS in pathophysiological conditions

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

(Nova Science Publishers, 2018)

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

PCSK9 and Hypercholesterolemia: Therapeutic Approach

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

(2018)

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

The influence of oxo-bridged binuclear gold(III) complexes on Na/K-ATPase activity: a joint experimental and theoretical approach

Bondžić, Aleksandra; Čolović, Mirjana B.; Janjić, Goran V.; Zarić, Božidarka; Petrović, Sandra; Krstić, Danijela Z.; Marzo, Tiziano; Messori, Luigi; Vasić, Vesna M.

(2017)

TY  - JOUR
AU  - Bondžić, Aleksandra
AU  - Čolović, Mirjana B.
AU  - Janjić, Goran V.
AU  - Zarić, Božidarka
AU  - Petrović, Sandra
AU  - Krstić, Danijela Z.
AU  - Marzo, Tiziano
AU  - Messori, Luigi
AU  - Vasić, Vesna M.
PY  - 2017
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/1648
AB  - The in vitro effects of oxo-bridged binuclear gold(III) complexes, i.e., [(bipy2Me)(2)Au-2(mu-O)(2)][PF6](2) (Auoxo6), Au-2[(bipydmb-H)(2)(mu-O)][PF6] (Au(2)bipyC) and [Au-2(phen(2Me))(2)(mu-O)(2)](PF6)(2) (Au(2)phen) on Na/K-ATPase, purified from the porcine cerebral cortex, were investigated. All three studied gold complexes inhibited the enzyme activity in a concentration-dependent manner achieving IC50 values in the low micromolar range. Kinetic analysis suggested an uncompetitive mode of inhibition for Auoxo6 and Au(2)bipyC, and a mixed type one for Au(2)phen. Docking studies indicated that the inhibitory actions of all tested complexes are related to E2-P enzyme conformation binding to ion channel and intracellular part between N and P sub-domain. In addition, Au(2)phen was able to inhibit the enzyme by interacting with its extracellular part as well. Toxic effects of the gold(III) complexes were evaluated in vitro by following lactate dehydrogenase activity in rat brain synaptosomes and incidence of micronuclei and cytokinesis-block proliferation index in cultivated human lymphocytes. All investigated complexes turned out to induce cytogenetic damage consisting of a significant decrease in cell proliferation and an increase in micronuclei in a dose-dependent manner. On the other hand, lactate dehydrogenase activity, an indicator of membrane integrity/viability, was not affected by Auoxo6 and Au(2)bipyC, while Au(2)phen slightly modified its activity.
T2  - Journal of Biological Inorganic Chemistry
T1  - The influence of oxo-bridged binuclear gold(III) complexes on Na/K-ATPase activity: a joint experimental and theoretical approach
VL  - 22
IS  - 6
SP  - 819
EP  - 832
DO  - 10.1007/s00775-017-1460-5
ER  - 
@article{
author = "Bondžić, Aleksandra and Čolović, Mirjana B. and Janjić, Goran V. and Zarić, Božidarka and Petrović, Sandra and Krstić, Danijela Z. and Marzo, Tiziano and Messori, Luigi and Vasić, Vesna M.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1648",
abstract = "The in vitro effects of oxo-bridged binuclear gold(III) complexes, i.e., [(bipy2Me)(2)Au-2(mu-O)(2)][PF6](2) (Auoxo6), Au-2[(bipydmb-H)(2)(mu-O)][PF6] (Au(2)bipyC) and [Au-2(phen(2Me))(2)(mu-O)(2)](PF6)(2) (Au(2)phen) on Na/K-ATPase, purified from the porcine cerebral cortex, were investigated. All three studied gold complexes inhibited the enzyme activity in a concentration-dependent manner achieving IC50 values in the low micromolar range. Kinetic analysis suggested an uncompetitive mode of inhibition for Auoxo6 and Au(2)bipyC, and a mixed type one for Au(2)phen. Docking studies indicated that the inhibitory actions of all tested complexes are related to E2-P enzyme conformation binding to ion channel and intracellular part between N and P sub-domain. In addition, Au(2)phen was able to inhibit the enzyme by interacting with its extracellular part as well. Toxic effects of the gold(III) complexes were evaluated in vitro by following lactate dehydrogenase activity in rat brain synaptosomes and incidence of micronuclei and cytokinesis-block proliferation index in cultivated human lymphocytes. All investigated complexes turned out to induce cytogenetic damage consisting of a significant decrease in cell proliferation and an increase in micronuclei in a dose-dependent manner. On the other hand, lactate dehydrogenase activity, an indicator of membrane integrity/viability, was not affected by Auoxo6 and Au(2)bipyC, while Au(2)phen slightly modified its activity.",
journal = "Journal of Biological Inorganic Chemistry",
title = "The influence of oxo-bridged binuclear gold(III) complexes on Na/K-ATPase activity: a joint experimental and theoretical approach",
volume = "22",
number = "6",
pages = "819-832",
doi = "10.1007/s00775-017-1460-5"
}
3
3
3

Link between Metabolic Syndrome and Insulin Resistance

Gluvić, Zoran; Zarić, Božidarka; Resanović, Ivana; Obradović, Milan M.; Mitrovic, Aleksandar; Radak, Đorđe J.; Isenović, Esma R.

(2017)

@article{
author = "Gluvić, Zoran and Zarić, Božidarka and Resanović, Ivana and Obradović, Milan M. and Mitrovic, Aleksandar and Radak, Đorđe J. and Isenović, Esma R.",
year = "2017",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/1470",
abstract = "Metabolic syndrome (MetS) is a leading public health and clinical challenge worldwide. MetS represents a group of interrelated risk factors that predict cardiovascular diseases (CVD) and diabetes mellitus (DM). Its prevalence ranges between 10 and 84%, depending on the geographic region, urban or rural environment, individual demographic characteristics of the population studied (sex, age, racial and ethnic origin), as well as the criteria used to define MetS. Persons with MetS have higher mortality rate when compared with people without MetS, primarily caused by progressive atherosclerosis, accelerated by pro-inflammatory and pro-coagulation components of MetS. Considering the high prevalence of metabolic disorders (glucose metabolism disorder, hypertension, dyslipidaemia, obesity etc.), preventive healthcare should focus on changing lifestyle in order to reduce obesity and increase physical activity. This narrative review considers the available evidence from clinical and experimental studies dealing with MetS, and current treatment options for patients with insulin resistance and MetS.",
journal = "Current Vascular Pharmacology",
title = "Link between Metabolic Syndrome and Insulin Resistance",
volume = "15",
number = "1",
pages = "30-39",
doi = "10.2174/1570161114666161007164510"
}
1
30
24
27

Benefits of L-Arginine on Cardiovascular System

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

(2016)

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

Ghrelin, obesity and atherosclerosis

Sudar, Emina; Soskić, Sanja S.; Zarić, Božidarka; Rašić-Milutinović, Zorica; Smiljanić, Katarina; Radak, Đorđe J.; Mikhailidis, Dimitri P.; Rizzo, Manfredi; Isenović, Esma R.

(2012)

TY  - CHAP
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Zarić, Božidarka
AU  - Rašić-Milutinović, Zorica
AU  - Smiljanić, Katarina
AU  - Radak, Đorđe J.
AU  - Mikhailidis, Dimitri P.
AU  - Rizzo, Manfredi
AU  - Isenović, Esma R.
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/8685
AB  - Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.
T2  - Ghrelin: Production, Action Mechanisms and Physiological Effects
T1  - Ghrelin, obesity and atherosclerosis
SP  - 111
EP  - 126
ER  - 
@article{
author = "Sudar, Emina and Soskić, Sanja S. and Zarić, Božidarka and Rašić-Milutinović, Zorica and Smiljanić, Katarina and Radak, Đorđe J. and Mikhailidis, Dimitri P. and Rizzo, Manfredi and Isenović, Esma R.",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/8685",
abstract = "Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.",
journal = "Ghrelin: Production, Action Mechanisms and Physiological Effects",
title = "Ghrelin, obesity and atherosclerosis",
pages = "111-126"
}

Non-canonical interactions of porphyrins in porphyrin-containing proteins

Stojanovic, Srdan D.; Isenović, Esma R.; Zarić, Božidarka

(2012)

TY  - JOUR
AU  - Stojanovic, Srdan D.
AU  - Isenović, Esma R.
AU  - Zarić, Božidarka
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5045
AB  - In this study we have described the non-canonical interactions between the porphyrin ring and the protein part of porphyrin-containing proteins to better understand their stabilizing role. The analysis reported in this study shows that the predominant type of non-canonical interactions at porphyrins are CH center dot center dot center dot O and CH center dot center dot center dot N interactions, with a small percentage of CH center dot center dot center dot pi and non-canonical interactions involving sulfur atoms. The majority of non-canonical interactions are formed from side-chains of charged and polar amino acids, whereas backbone groups are not frequently involved. The main-chain non-canonical interactions might be slightly more linear than the side-chain interactions, and they have somewhat shorter median distances. The analysis, performed in this study, shows that about 44% of the total interactions in the dataset are involved in the formation of multiple (furcated) non-canonical interactions. The high number of porphyrin-water interactions show importance of the inclusion of solvent in protein-ligand interaction studies. Furthermore, in the present study we have observed that stabilization centers are composed predominantly from nonpolar amino acid residues. Amino acids deployed in the environment of porphyrin rings are deposited in helices and coils. The results from this study might be used for structure-based porphyrin protein prediction and as scaffolds for future porphyrin-containing protein design.
T2  - Amino Acids
T1  - Non-canonical interactions of porphyrins in porphyrin-containing proteins
VL  - 43
IS  - 4
SP  - 1535
EP  - 1546
DO  - 10.1007/s00726-012-1228-8
ER  - 
@article{
author = "Stojanovic, Srdan D. and Isenović, Esma R. and Zarić, Božidarka",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5045",
abstract = "In this study we have described the non-canonical interactions between the porphyrin ring and the protein part of porphyrin-containing proteins to better understand their stabilizing role. The analysis reported in this study shows that the predominant type of non-canonical interactions at porphyrins are CH center dot center dot center dot O and CH center dot center dot center dot N interactions, with a small percentage of CH center dot center dot center dot pi and non-canonical interactions involving sulfur atoms. The majority of non-canonical interactions are formed from side-chains of charged and polar amino acids, whereas backbone groups are not frequently involved. The main-chain non-canonical interactions might be slightly more linear than the side-chain interactions, and they have somewhat shorter median distances. The analysis, performed in this study, shows that about 44% of the total interactions in the dataset are involved in the formation of multiple (furcated) non-canonical interactions. The high number of porphyrin-water interactions show importance of the inclusion of solvent in protein-ligand interaction studies. Furthermore, in the present study we have observed that stabilization centers are composed predominantly from nonpolar amino acid residues. Amino acids deployed in the environment of porphyrin rings are deposited in helices and coils. The results from this study might be used for structure-based porphyrin protein prediction and as scaffolds for future porphyrin-containing protein design.",
journal = "Amino Acids",
title = "Non-canonical interactions of porphyrins in porphyrin-containing proteins",
volume = "43",
number = "4",
pages = "1535-1546",
doi = "10.1007/s00726-012-1228-8"
}
12
12
12

Peroxisome Proliferator-Activated Receptors and Atherosclerosis

Soskić, Sanja S.; Dobutovic, Branislava D.; Sudar, Emina; Obradović, Milan M.; Nikolić, Dragana; Zarić, Božidarka; Stojanovic, Srdan D.; Stokić, Edita; Mikhailidis, Dimitri P.; Isenović, Esma R.

(2011)

TY  - JOUR
AU  - Soskić, Sanja S.
AU  - Dobutovic, Branislava D.
AU  - Sudar, Emina
AU  - Obradović, Milan M.
AU  - Nikolić, Dragana
AU  - Zarić, Božidarka
AU  - Stojanovic, Srdan D.
AU  - Stokić, Edita
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4519
AB  - The peroxisome proliferator-activated receptors (PPARs) represent the family of 3 nuclear receptor isoforms-PPAR alpha, -gamma, and -delta/beta, which are encoded by different genes. As lipid sensors, they are primarily involved in regulation of lipid metabolism and subsequently in inflammation and atherosclerosis. Atherosclerosis considers accumulation of the cells and extracellular matrix in the vessel wall leading to the formation of atherosclerotic plaque, atherothrombosis, and other vascular complications. Besides existence of natural ligands for PPARs, their more potent synthetic ligands are fibrates and thiazolidindiones. Future investigations should now focus on the mechanisms of PPARs activation, which might present new approaches involved in the antiatherosclerotic effects revealed in this review. In addition, in this review we are presenting latest data from recent performed clinical studies which have focus on novel approach to PPARs agonists as potential therapeutic agents in the treatment of complex disease such as atherosclerosis.
T2  - Angiology
T1  - Peroxisome Proliferator-Activated Receptors and Atherosclerosis
VL  - 62
IS  - 7
SP  - 523
EP  - 534
DO  - 10.1177/0003319711401012
ER  - 
@article{
author = "Soskić, Sanja S. and Dobutovic, Branislava D. and Sudar, Emina and Obradović, Milan M. and Nikolić, Dragana and Zarić, Božidarka and Stojanovic, Srdan D. and Stokić, Edita and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4519",
abstract = "The peroxisome proliferator-activated receptors (PPARs) represent the family of 3 nuclear receptor isoforms-PPAR alpha, -gamma, and -delta/beta, which are encoded by different genes. As lipid sensors, they are primarily involved in regulation of lipid metabolism and subsequently in inflammation and atherosclerosis. Atherosclerosis considers accumulation of the cells and extracellular matrix in the vessel wall leading to the formation of atherosclerotic plaque, atherothrombosis, and other vascular complications. Besides existence of natural ligands for PPARs, their more potent synthetic ligands are fibrates and thiazolidindiones. Future investigations should now focus on the mechanisms of PPARs activation, which might present new approaches involved in the antiatherosclerotic effects revealed in this review. In addition, in this review we are presenting latest data from recent performed clinical studies which have focus on novel approach to PPARs agonists as potential therapeutic agents in the treatment of complex disease such as atherosclerosis.",
journal = "Angiology",
title = "Peroxisome Proliferator-Activated Receptors and Atherosclerosis",
volume = "62",
number = "7",
pages = "523-534",
doi = "10.1177/0003319711401012"
}
17
22
25

Contribution of Non-Canonical Interactions to the Stability of Sm/LSm Oligomeric Assemblies

Stojanovic, Srdan D.; Isenović, Esma R.; Zarić, Božidarka

(2011)

TY  - JOUR
AU  - Stojanovic, Srdan D.
AU  - Isenović, Esma R.
AU  - Zarić, Božidarka
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4381
AB  - The distinguishing property of Sm/LSm protein assemblies is their high stability. In order to better understand the nature of Sm/LSm protein oligomers in this study we have analyzed the contribution of non-canonical interactions to the stability of assemblies. The predominant types of non-canonical interactions at Sm/LSm protein interfaces are CH center dot center dot center dot O, and CH center dot center dot center dot N interactions represented at interfaces. Our results show low percentages of XH-pi and non-canonical interactions involving sulfur atoms, while the backbone groups were less frequently involved. The data show a high percentage of non-canonical interactions in interfaces formed by charged residues with Lys and Arg, these being the major charged donors. The main chain non-canonical interactions might be slightly more linear than the side chain interactions, and they have somewhat shorter median distances. Comparing the stabilizing amino acid residues with amino acids which build non-canonical interactions at interfaces shows that certain amino acids like Phe, Pro, His and Tyr are involved with a high percentage. The high conservation score of amino acids that are involved in non-canonical interactions in protein interfaces is an additional strong argument for their importance in the stabilization of Sm/LSm protein assemblies.
T2  - Molecular Informatics
T1  - Contribution of Non-Canonical Interactions to the Stability of Sm/LSm Oligomeric Assemblies
VL  - 30
IS  - 5
SP  - 430
EP  - 442
DO  - 10.1002/minf.201000176
ER  - 
@article{
author = "Stojanovic, Srdan D. and Isenović, Esma R. and Zarić, Božidarka",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4381",
abstract = "The distinguishing property of Sm/LSm protein assemblies is their high stability. In order to better understand the nature of Sm/LSm protein oligomers in this study we have analyzed the contribution of non-canonical interactions to the stability of assemblies. The predominant types of non-canonical interactions at Sm/LSm protein interfaces are CH center dot center dot center dot O, and CH center dot center dot center dot N interactions represented at interfaces. Our results show low percentages of XH-pi and non-canonical interactions involving sulfur atoms, while the backbone groups were less frequently involved. The data show a high percentage of non-canonical interactions in interfaces formed by charged residues with Lys and Arg, these being the major charged donors. The main chain non-canonical interactions might be slightly more linear than the side chain interactions, and they have somewhat shorter median distances. Comparing the stabilizing amino acid residues with amino acids which build non-canonical interactions at interfaces shows that certain amino acids like Phe, Pro, His and Tyr are involved with a high percentage. The high conservation score of amino acids that are involved in non-canonical interactions in protein interfaces is an additional strong argument for their importance in the stabilization of Sm/LSm protein assemblies.",
journal = "Molecular Informatics",
title = "Contribution of Non-Canonical Interactions to the Stability of Sm/LSm Oligomeric Assemblies",
volume = "30",
number = "5",
pages = "430-442",
doi = "10.1002/minf.201000176"
}
4
3
5

A novel hypothesis regarding the possible involvement of cytosolic phospholipase 2 in insulin-stimulated proliferation of vascular smooth muscle cells

Isenović, Esma R.; Fretaud, Maxence; Dobutovic, Branislava; Sudar, Emina; Smiljanić, Katarina; Zarić, Božidarka; Trpković, Andreja; Marche, Pierre

(2009)

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Fretaud, Maxence
AU  - Dobutovic, Branislava
AU  - Sudar, Emina
AU  - Smiljanić, Katarina
AU  - Zarić, Božidarka
AU  - Trpković, Andreja
AU  - Marche, Pierre
PY  - 2009
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3644
AB  - Insulin (INS) via INS receptor acts as a mitogen in vascular smooth muscle cells (VSMCs) through stimulation of multiple signaling mechanisms, including p42/44 mitogen-activated protein kinase (ERK1/2) and phosphatidyl inositol-3 kinase (PI3K). In addition, cytosolic phospholipase 2 (cPLA(2)) is linked to VSMCs proliferation. However, the upstream mechanisms responsible for activation of cPLA(2) are not well defined. Therefore, this investigation used primary cultured rat VSMCs to examine the role of PI3K and ERK1/2 in the INS-dependent phosphorylation of cPLA(2) and proliferation induced by INS. Exposure of VSMCs to INS (100 nM) for 10 min increased the phosphorylation of cPLA(2) by 1.5-fold (p LT 0.01), which was blocked by the cPLA(2) inhibitor MAFP (10 mu M; 15 min). Similarly, the PI3K inhibitor LY294002 (10 mu M; 15 min) and ERK1/2 inhibitor PD98059 (20 mu M; 15 min) abolished the INS-mediated increase in cPLA(2) phosphorylation by 59% (p LT 0.001), and by 75% (p LT 0.001), respectively. Further, inhibition of cPLA2 with cPLA2 inhibitor MAFP abolished the INS-stimulated ERK1/2 phosphorylation by 65% (p LT 0.01). Incubation of rat VSMCs with INS resulted in an increase of VSMCs proliferation by 85% (p LT 0.001). The effect of INS on VSMCs proliferation was significantly (p LT 0.01) reduced by pretreatment with MAFP. Thus, we hypothesized that INS stimulates VSMCs proliferation via a mechanism involving the PI3K-dependent activation of cPLA(2) and release of arachidonic acid (AA), which activates ERK1/2 and further amplifies cPLA(2) activity. (C) 2009 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.
T2  - Cell Biology International
T1  - A novel hypothesis regarding the possible involvement of cytosolic phospholipase 2 in insulin-stimulated proliferation of vascular smooth muscle cells
VL  - 33
IS  - 3
SP  - 386
EP  - 392
DO  - 10.1016/j.cellbi.2009.01.010
ER  - 
@article{
author = "Isenović, Esma R. and Fretaud, Maxence and Dobutovic, Branislava and Sudar, Emina and Smiljanić, Katarina and Zarić, Božidarka and Trpković, Andreja and Marche, Pierre",
year = "2009",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3644",
abstract = "Insulin (INS) via INS receptor acts as a mitogen in vascular smooth muscle cells (VSMCs) through stimulation of multiple signaling mechanisms, including p42/44 mitogen-activated protein kinase (ERK1/2) and phosphatidyl inositol-3 kinase (PI3K). In addition, cytosolic phospholipase 2 (cPLA(2)) is linked to VSMCs proliferation. However, the upstream mechanisms responsible for activation of cPLA(2) are not well defined. Therefore, this investigation used primary cultured rat VSMCs to examine the role of PI3K and ERK1/2 in the INS-dependent phosphorylation of cPLA(2) and proliferation induced by INS. Exposure of VSMCs to INS (100 nM) for 10 min increased the phosphorylation of cPLA(2) by 1.5-fold (p LT 0.01), which was blocked by the cPLA(2) inhibitor MAFP (10 mu M; 15 min). Similarly, the PI3K inhibitor LY294002 (10 mu M; 15 min) and ERK1/2 inhibitor PD98059 (20 mu M; 15 min) abolished the INS-mediated increase in cPLA(2) phosphorylation by 59% (p LT 0.001), and by 75% (p LT 0.001), respectively. Further, inhibition of cPLA2 with cPLA2 inhibitor MAFP abolished the INS-stimulated ERK1/2 phosphorylation by 65% (p LT 0.01). Incubation of rat VSMCs with INS resulted in an increase of VSMCs proliferation by 85% (p LT 0.001). The effect of INS on VSMCs proliferation was significantly (p LT 0.01) reduced by pretreatment with MAFP. Thus, we hypothesized that INS stimulates VSMCs proliferation via a mechanism involving the PI3K-dependent activation of cPLA(2) and release of arachidonic acid (AA), which activates ERK1/2 and further amplifies cPLA(2) activity. (C) 2009 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.",
journal = "Cell Biology International",
title = "A novel hypothesis regarding the possible involvement of cytosolic phospholipase 2 in insulin-stimulated proliferation of vascular smooth muscle cells",
volume = "33",
number = "3",
pages = "386-392",
doi = "10.1016/j.cellbi.2009.01.010"
}
4
4
5

Cell culture conditions potentiate differences in the response to ionising radiation of peripheral blood leukocytes isolated from breast cancer patients and healthy subjects

Adžić, Miroslav; Niciforovic, Ana; Zarić, Božidarka; Neskovic-Konstatinovic, Zora; Spasić, Snežana D.; Jones, David R.; Radoičić, Marija B.

(2008)

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Niciforovic, Ana
AU  - Zarić, Božidarka
AU  - Neskovic-Konstatinovic, Zora
AU  - Spasić, Snežana D.
AU  - Jones, David R.
AU  - Radoičić, Marija B.
PY  - 2008
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3490
AB  - To compare the effects of ionising radiation on leukocytes from breast cancer patients and healthy subjects ex vivo, the level of NF-kappa B and the antioxidant enzymes manganese-containing superoxide dismutase (Mn-SOD), copper/zinc-containing superoxide dismutase (CuZn-SOD) and catalase (CAT) in combination with flow cytometric analysis of CD4(+) lymphocytes was performed. The level of Mn-SOD protein was significantly increased in the breast cancer study group both before (P LT 0.001) and after (P LT 0.001) irradiation when compared with healthy subjects. Measurements in parallel indicated that the level of CAT protein was significantly higher in the breast cancer study group after irradiation (2 Gy [P LT 0.001] and 9 Gy [P LT 0.05]) when compared with healthy subjects. Although the initial number of lymphocytes in the blood of breast cancer patients was not different from healthy subjects, the percentage of apoptotic CD4(+) cells was significantly (P LT 0.001) lower both before and after irradiation indicating that cell culture conditions induced radioresistance of CD4(+) cells in the blood of breast cancer patients. The data presented in this current study indicate that brief ex vivo culture of peripheral blood leukocytes potentiates oxidative stress imposed by a breast cancer tumour.
T2  - Redox Report
T1  - Cell culture conditions potentiate differences in the response to ionising radiation of peripheral blood leukocytes isolated from breast cancer patients and healthy subjects
VL  - 13
IS  - 1
SP  - 17
EP  - 22
DO  - 10.1179/135100008X259088
ER  - 
@article{
author = "Adžić, Miroslav and Niciforovic, Ana and Zarić, Božidarka and Neskovic-Konstatinovic, Zora and Spasić, Snežana D. and Jones, David R. and Radoičić, Marija B.",
year = "2008",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3490",
abstract = "To compare the effects of ionising radiation on leukocytes from breast cancer patients and healthy subjects ex vivo, the level of NF-kappa B and the antioxidant enzymes manganese-containing superoxide dismutase (Mn-SOD), copper/zinc-containing superoxide dismutase (CuZn-SOD) and catalase (CAT) in combination with flow cytometric analysis of CD4(+) lymphocytes was performed. The level of Mn-SOD protein was significantly increased in the breast cancer study group both before (P LT 0.001) and after (P LT 0.001) irradiation when compared with healthy subjects. Measurements in parallel indicated that the level of CAT protein was significantly higher in the breast cancer study group after irradiation (2 Gy [P LT 0.001] and 9 Gy [P LT 0.05]) when compared with healthy subjects. Although the initial number of lymphocytes in the blood of breast cancer patients was not different from healthy subjects, the percentage of apoptotic CD4(+) cells was significantly (P LT 0.001) lower both before and after irradiation indicating that cell culture conditions induced radioresistance of CD4(+) cells in the blood of breast cancer patients. The data presented in this current study indicate that brief ex vivo culture of peripheral blood leukocytes potentiates oxidative stress imposed by a breast cancer tumour.",
journal = "Redox Report",
title = "Cell culture conditions potentiate differences in the response to ionising radiation of peripheral blood leukocytes isolated from breast cancer patients and healthy subjects",
volume = "13",
number = "1",
pages = "17-22",
doi = "10.1179/135100008X259088"
}
1

Adjuvant antiproliferative and cytotoxic effect of aloin in irradiated HeLaS3 cells

Niciforovic, A.; Adžić, Miroslav; Zarić, Božidarka; Radoičić, Marija B.

(2007)

TY  - JOUR
AU  - Niciforovic, A.
AU  - Adžić, Miroslav
AU  - Zarić, Božidarka
AU  - Radoičić, Marija B.
PY  - 2007
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/6723
AB  - Naturally occurring phytoanthracycline, aloin, was used to radiosensitize HeLaS3 human cervix carcinoma cells. The results indicated that the cytotoxic adjuvant effect of aloin was synergistic with gammaionizing radiation at all drug concentrations and comparable to the cytotoxicity of 5-10 Gy ionizing radiation alone. Radiosensitization of HeLaS3 cells was achieved by 60 mu M aloin, which reduced the IC50 dose of ionizing radiation from 3.4 to 2 Gy. Ionizing radiation and aloin alone or in combination are shown to cause perturbation of the HeLaS3 cell-cycle and increase the percentage of cells in the DNA synthesis (S) phase of the cell cycle. While either of the agents applied alone causes programmed cell death by apoptosis, the simultaneous cell damage by both agents through the altered redox balance compromised cell capacity to conduct this program and led to synergic cytotoxic cell death by necrosis.
T2  - Russian Journal of Physical Chemistry A
T1  - Adjuvant antiproliferative and cytotoxic effect of aloin in irradiated HeLaS3 cells
VL  - 81
IS  - 9
SP  - 1463
EP  - 1466
DO  - 10.1134/S0036024407090221
ER  - 
@article{
author = "Niciforovic, A. and Adžić, Miroslav and Zarić, Božidarka and Radoičić, Marija B.",
year = "2007",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/6723",
abstract = "Naturally occurring phytoanthracycline, aloin, was used to radiosensitize HeLaS3 human cervix carcinoma cells. The results indicated that the cytotoxic adjuvant effect of aloin was synergistic with gammaionizing radiation at all drug concentrations and comparable to the cytotoxicity of 5-10 Gy ionizing radiation alone. Radiosensitization of HeLaS3 cells was achieved by 60 mu M aloin, which reduced the IC50 dose of ionizing radiation from 3.4 to 2 Gy. Ionizing radiation and aloin alone or in combination are shown to cause perturbation of the HeLaS3 cell-cycle and increase the percentage of cells in the DNA synthesis (S) phase of the cell cycle. While either of the agents applied alone causes programmed cell death by apoptosis, the simultaneous cell damage by both agents through the altered redox balance compromised cell capacity to conduct this program and led to synergic cytotoxic cell death by necrosis.",
journal = "Russian Journal of Physical Chemistry A",
title = "Adjuvant antiproliferative and cytotoxic effect of aloin in irradiated HeLaS3 cells",
volume = "81",
number = "9",
pages = "1463-1466",
doi = "10.1134/S0036024407090221"
}
9
11
10

Lsm proteins bind and stabilize RNAs containing 5 poly(A) tracts

Bergman, Naomi; Moraes, Karen C. M.; Anderson, John R.; Zarić, Božidarka; Kambach, Christian; Schneider, Robert J.; Wilusz, Carol J.; Wilusz, Jeffrey

(2007)

TY  - JOUR
AU  - Bergman, Naomi
AU  - Moraes, Karen C. M.
AU  - Anderson, John R.
AU  - Zarić, Božidarka
AU  - Kambach, Christian
AU  - Schneider, Robert J.
AU  - Wilusz, Carol J.
AU  - Wilusz, Jeffrey
PY  - 2007
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3277
AB  - Many orthopoxvirus messenger RNAs have an unusual nontemplated poly( A) tract of 5 to 40 residues at the 5 end. The precise function of this feature is unknown. Here we show that 5 poly( A) tracts are able to repress RNA decay by inhibiting 3 - to- 5 exonucleases as well as decapping of RNA substrates. UV cross- linking analysis demonstrated that the Lsm complex associates with the 5 poly( A) tract. Furthermore, recombinant Lsm1 - 7 complex specifically binds 5 poly( A) tracts 10 to 21 nucleotides in length, consistent with the length of 5 poly( A) required for stabilization. Knockdown of Lsm1 abrogates RNA stabilization by the 5 poly( A) tract. We propose that the Lsm complex simultaneously binds the 3 and 5 ends of these unusual messenger RNAs and thereby prevents 3 - to-5 decay. The implications of this phenomenon for cellular mRNA decay are discussed.
T2  - Nature Structural and Molecular Biology
T1  - Lsm proteins bind and stabilize RNAs containing 5 poly(A) tracts
VL  - 14
IS  - 9
SP  - 824
EP  - 831
DO  - 10.1038/nsmb1287
ER  - 
@article{
author = "Bergman, Naomi and Moraes, Karen C. M. and Anderson, John R. and Zarić, Božidarka and Kambach, Christian and Schneider, Robert J. and Wilusz, Carol J. and Wilusz, Jeffrey",
year = "2007",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3277",
abstract = "Many orthopoxvirus messenger RNAs have an unusual nontemplated poly( A) tract of 5 to 40 residues at the 5 end. The precise function of this feature is unknown. Here we show that 5 poly( A) tracts are able to repress RNA decay by inhibiting 3 - to- 5 exonucleases as well as decapping of RNA substrates. UV cross- linking analysis demonstrated that the Lsm complex associates with the 5 poly( A) tract. Furthermore, recombinant Lsm1 - 7 complex specifically binds 5 poly( A) tracts 10 to 21 nucleotides in length, consistent with the length of 5 poly( A) required for stabilization. Knockdown of Lsm1 abrogates RNA stabilization by the 5 poly( A) tract. We propose that the Lsm complex simultaneously binds the 3 and 5 ends of these unusual messenger RNAs and thereby prevents 3 - to-5 decay. The implications of this phenomenon for cellular mRNA decay are discussed.",
journal = "Nature Structural and Molecular Biology",
title = "Lsm proteins bind and stabilize RNAs containing 5 poly(A) tracts",
volume = "14",
number = "9",
pages = "824-831",
doi = "10.1038/nsmb1287"
}
32
31
30