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Trpković, Andreja

Link to this page

Authority KeyName Variants
68fbabd5-c485-435a-b8aa-1d8a7f7d6e96
  • Trpković, Andreja (19)
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 Cell Cycle Aberrations and the Impact of Oxidative Stress in Neurodegenerative Processes and Malignant Transformation of the Cell
Centre National de la Recherche Scientifique (CNRS) CNRS, University Pierre and Marie Curie, Ministry of Science, Republic of Serbia [143030B], French Ministry of Foreign Affairs [337-00-359/2005-01/16]
CNRS, University Pierre and Marie Curie, Ministry of Science, Republic of Serbia [143030B], Pavle Savic [337-00-359/2005-01/16], Republic of France, Ministry of Foreign Affairs Thin films of single wall carbon nanotubes and graphene for electronic application
Detection of early laboratory fungal biomarkers and it's importance for outcome of invasive fungal infections in Serbia Carotid disease in Serbia - pathologic dynamics, prevention, diagnostics and inovative therapeutic methods
Modulation of intracellular energy balance-controlling signalling pathways in therapy of cancer and neuro-immuno-endocrine disorders KAUST Base Research Fund [BAS/1/1606‐01‐01]
KAUST Office of Sponsored Research (OSR) Award [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] Ministry of Science and Technological Development of the Republic of Serbia [145073]
Pavle Savic [337-00-359/2005-01/16], Republic of France, Ministry of Foreign Affairs University Pierre and Marie Curie

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

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

Literature-Based Enrichment Insights into Redox Control of Vascular Biology

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

(2019)

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

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

High-Sensitivity C-Reactive Protein and Statin Initiation

Trpković, Andreja; Stanimirović, Julijana; Rizzo, Manfredi; Resanović, Ivana; Soskić, Sanja S.; Jevremovic, Danimir; Isenović, Esma R.

(2015)

@article{
author = "Trpković, Andreja and Stanimirović, Julijana and Rizzo, Manfredi and Resanović, Ivana and Soskić, Sanja S. and Jevremovic, Danimir and Isenović, Esma R.",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/613",
abstract = "The assessment of cardiovascular risk and treatment of cardiovascular diseases are major public health issues worldwide. Inflammation is now recognized as a key regulatory process that links multiple risk factors for atherosclerosis. The substantial number of patients having cardiovascular events lack commonly established risk factors. The utility of high-sensitivity C-reactive protein (hsCRP), a circulating biomarker related to inflammation, may provide additional information in risk prediction. This review will consider the impact of hsCRP level on initiation of statin therapy.",
journal = "Angiology",
title = "High-Sensitivity C-Reactive Protein and Statin Initiation",
volume = "66",
number = "6",
pages = "503-507",
doi = "10.1177/0003319714543000"
}
1
2

High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction

Trpković, Andreja; Stanimirović, Julijana; Resanović, Ivana; Otasevic, Petar; Jevremovic, Danimir; Radak, Đorđe J.; Isenović, Esma R.

(2015)

TY  - JOUR
AU  - Trpković, Andreja
AU  - Stanimirović, Julijana
AU  - Resanović, Ivana
AU  - Otasevic, Petar
AU  - Jevremovic, Danimir
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/312
AB  - It is now recognized that inflammatory processes regulate all stages of atherosclerosis, from disease initiation to thrombotic complications. C-reactive protein (CRP) is a plasmatic protein used as a general marker of inflammation. The high sensitivity C-reactive protein (hsCRP) refers to the measurement of CRP in blood samples using assays with sufficient sensitivity to quantify low (baseline) levels of this biomarker. Low-grade chronic inflammatory processes are linked to atherosclerosis and may be screened with the use of hsCRP, thus providing additional information in cardiovascular risk prediction. This review elaborates the role of CRP in atherogenesis and the value of hsCRP as a biomarker in cardiovascular risk prediction in both primary and secondary prevention setting.
T2  - Current Pharmaceutical Analysis
T1  - High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction
VL  - 11
IS  - 1
SP  - 60
EP  - 65
ER  - 
@article{
author = "Trpković, Andreja and Stanimirović, Julijana and Resanović, Ivana and Otasevic, Petar and Jevremovic, Danimir and Radak, Đorđe J. and Isenović, Esma R.",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/312",
abstract = "It is now recognized that inflammatory processes regulate all stages of atherosclerosis, from disease initiation to thrombotic complications. C-reactive protein (CRP) is a plasmatic protein used as a general marker of inflammation. The high sensitivity C-reactive protein (hsCRP) refers to the measurement of CRP in blood samples using assays with sufficient sensitivity to quantify low (baseline) levels of this biomarker. Low-grade chronic inflammatory processes are linked to atherosclerosis and may be screened with the use of hsCRP, thus providing additional information in cardiovascular risk prediction. This review elaborates the role of CRP in atherogenesis and the value of hsCRP as a biomarker in cardiovascular risk prediction in both primary and secondary prevention setting.",
journal = "Current Pharmaceutical Analysis",
title = "High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction",
volume = "11",
number = "1",
pages = "60-65"
}

Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases

Trpković, Andreja; Resanović, Ivana; Stanimirović, Julijana; Radak, Đorđe J.; Mousa, Shaker A.; Cenic-Milosevic, Desanka; Jevremovic, Danimir; Isenović, Esma R.

(2015)

@article{
author = "Trpković, Andreja and Resanović, Ivana and Stanimirović, Julijana and Radak, Đorđe J. and Mousa, Shaker A. and Cenic-Milosevic, Desanka and Jevremovic, Danimir and Isenović, Esma R.",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/635",
abstract = "Atherosclerosis is a life-long illness that begins with risk factors, which in turn contribute to the development of subclinical disease, followed by the establishment of overt cardiovascular disease (CVD). Thrombotic-occlusive complications of atherosclerosis are among the most widespread and costly health problems. Oxidized low-density lipoprotein (OxLDL) plays an important role in atherogenesis by promoting an inflammatory environment and lipid deposition in the arterial wall. As cardiovascular events occur in individuals without common risk factors, there is a need for additional tools that may help in CVD risk assessment and management. The use of biomarkers has improved diagnostic, therapeutic and prognostic outcome in cardiovascular medicine. This review elaborates on the value of circulating OxLDL as a biomarker of CVD. Three enzyme-linked immunosorbent assays (4E6, DLH3 and E06) using murine monoclonal antibodies for determination of OxLDL blood levels have been developed. However, none of these assays are currently approved for routine clinical practice. We identified studies investigating OxLDL in CVD (measured by 4E6, DLH3 or E06 assay) by searching the PubMed database. Circulating OxLDL was found to be associated with all stages of atherosclerosis, from early atherogenesis to hypertension, coronary and peripheral arterial disease, acute coronary syndromes and ischemic cerebral infarction. The results of studies investigating the usefulness of OxLDL for CVD prediction were also summarized. Furthermore, OxLDL was found to be associated with pathologic conditions linked to CVD, including diabetes mellitus, obesity and metabolic syndrome (MetS). In addition, we have addressed the mechanisms by which OxLDL promotes atherogenesis, and the effects of antiatherogenic treatments on circulating OxLDL. Finally, we highlight the evidence suggesting that lipoprotein (a) [ Lp(a)] is the preferential carrier of oxidized phospholipids (OxPL) in human plasma. A strong association between OxPLapoB level (representing the content of OxPL on apolipoprotein B-100 particles, measured by E06 assay) and Lp(a) has been determined.",
journal = "Critical Reviews in Clinical Laboratory Sciences",
title = "Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases",
volume = "52",
number = "2",
pages = "70-85",
doi = "10.3109/10408363.2014.992063"
}
21
130
127
125

Interrelatedness between C-reactive protein and oxidized low-density lipoprotein

Obradović, Milan M.; Trpković, Andreja; Bajić, Vladan P.; Soskić, Sanja S.; Jovanović, Aleksandra; Stanimirović, Julijana; Panic, Milos; Isenović, Esma R.

(2015)

@article{
author = "Obradović, Milan M. and Trpković, Andreja and Bajić, Vladan P. and Soskić, Sanja S. and Jovanović, Aleksandra and Stanimirović, Julijana and Panic, Milos and Isenović, Esma R.",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/281",
abstract = "C-reactive protein (CRP) is a marker of inflammation. Atherosclerosis is now recognized as inflammatory disease, and it seems that CRP directly contributes to atherogenesis. Oxidation of low-density lipoprotein (LDL) molecule increases the uptake of lipid products by macrophages leading to cholesterol accumulation and subsequent foam cell formation. The elevated levels of high sensitivity CRP (hsCRP) and oxidized LDL (OxLDL) in the blood were found to be associated with cardiovascular diseases (CVD). In this review, we highlighted the evidence that CRP and OxLDL are involved in interrelated (patho) physiological pathways. The findings on association between hsCRP and OxLDL in the clinical setting will be also summarized.",
journal = "Clinical Chemistry and Laboratory Medicine",
title = "Interrelatedness between C-reactive protein and oxidized low-density lipoprotein",
volume = "53",
number = "1",
pages = "29-34",
doi = "10.1515/cclm-2014-0590"
}
3
14
8
11

Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress

Trpković, Andreja; Todorović-Marković, Biljana; Trajković, Vladimir S.

(2012)

@article{
author = "Trpković, Andreja and Todorović-Marković, Biljana and Trajković, Vladimir S.",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5156",
abstract = "The fullerene C-60, due to the physicochemical properties of its spherical cage-like molecule build exclusively from carbon atoms, is able to both scavenge and generate reactive oxygen species. While this unique dual property could be exploited in biomedicine, the low water solubility of C-60 hampers the investigation of its behavior in biological systems. The C-60 can be brought into water by solvent extraction, by complexation with surfactants/polymers, or by long-term stirring, yielding pristine (unmodified) fullerene suspensions. On the other hand, a modification of the C-60 core by the attachment of various functional groups results in the formation of water-soluble fullerene derivatives. Assessment of toxicity associated with C-60 preparations is of pivotal importance for their biomedical application as cytoprotective (antioxidant), cytotoxic (anticancer), or drug delivery agents. Moreover, the widespread industrial utilization of fullerenes may also have implications for human health. However, the alterations in physicochemical properties imposed by the utilization of different methods for C-60 solubilization profoundly influence toxicological effects of fullerene preparations, thus making the analysis of their potential therapeutic and environmental toxicity difficult. This review provides a comprehensive evaluation of the in vitro and in vivo toxicity of fullerenes, focusing on the comparison between pristine and derivatized C-60 preparations and the mechanisms of their toxicity to mammalian cells and tissues.",
journal = "Archives of Toxicology",
title = "Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress",
volume = "86",
number = "12",
pages = "1809-1827",
doi = "10.1007/s00204-012-0859-6"
}
60
59
65

In vitro antifungal activities of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole against Cryptococcus neoformans isolated from cerebrospinal fluid and blood from patients in Serbia

Trpković, Andreja; Pekmezovic, M.; Barac, A.; Radovic, L. Crncevic; Arsenijević, V. Arsic

(2012)

TY  - JOUR
AU  - Trpković, Andreja
AU  - Pekmezovic, M.
AU  - Barac, A.
AU  - Radovic, L. Crncevic
AU  - Arsenijević, V. Arsic
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5128
AB  - Recently, geographic variations in resistance to agents commonly used in the treatment of cryptococcosis have been reported. Therefore, the antifungal susceptibilities of 31 clinical isolates of Cryptococcus neoformans, collected in Serbia during 10-year period, were investigated. Strains were isolated from cerebrospinal fluid (n = 28) and blood (n = 3), from patients with AIDS (n = 26), lymphoma (n = 4) and kidney transplant recipient (n = 1). The minimal inhibitory concentrations (MICs) of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole were determined by the E-test (R) method. The isolates were highly susceptible to amphotericin B (100% susceptibility at MIC LT 0.5 mu g/mL) and 5-fluorocytosine (87.1% susceptibility at MIC LT = 4 mu g/mL). Geometric mean MIC of amphotericin B and 5-fluorocytosine were 0.102 mu g/mL and 0.396 mu g/mL, respectively. Fluconazole exhibited the lowest activity in vitro (48.4% susceptibility at MIC LT = 8 mu g/mL) with a significant resistance rate. The activity of itraconazole was also decreased (48.4% susceptibility at MIC LT = 0.25 mu g/mL). The geometric mean MIC of fiuconazole stood at 15.14 mu g/mL and of itraconazole was 0.144 mu g/mL. Cross-resistance among azoles was not common (3.2%), but the parallel increase in fluconazole and itraconazole MIC has been observed (P LT 0.01). The low rate of susceptibility to fluconazole stresses the need for active antifungal surveillance of C. neoformans and of the corresponding data from different geographic regions. (C) 2012 Elsevier Masson SAS. All rights reserved.
T2  - Journal de Mycologie Medicale
T1  - In vitro antifungal activities of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole against Cryptococcus neoformans isolated from cerebrospinal fluid and blood from patients in Serbia
VL  - 22
IS  - 3
SP  - 243
EP  - 248
DO  - 10.1016/j.mycmed.2012.06.002
ER  - 
@article{
author = "Trpković, Andreja and Pekmezovic, M. and Barac, A. and Radovic, L. Crncevic and Arsenijević, V. Arsic",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5128",
abstract = "Recently, geographic variations in resistance to agents commonly used in the treatment of cryptococcosis have been reported. Therefore, the antifungal susceptibilities of 31 clinical isolates of Cryptococcus neoformans, collected in Serbia during 10-year period, were investigated. Strains were isolated from cerebrospinal fluid (n = 28) and blood (n = 3), from patients with AIDS (n = 26), lymphoma (n = 4) and kidney transplant recipient (n = 1). The minimal inhibitory concentrations (MICs) of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole were determined by the E-test (R) method. The isolates were highly susceptible to amphotericin B (100% susceptibility at MIC LT 0.5 mu g/mL) and 5-fluorocytosine (87.1% susceptibility at MIC LT = 4 mu g/mL). Geometric mean MIC of amphotericin B and 5-fluorocytosine were 0.102 mu g/mL and 0.396 mu g/mL, respectively. Fluconazole exhibited the lowest activity in vitro (48.4% susceptibility at MIC LT = 8 mu g/mL) with a significant resistance rate. The activity of itraconazole was also decreased (48.4% susceptibility at MIC LT = 0.25 mu g/mL). The geometric mean MIC of fiuconazole stood at 15.14 mu g/mL and of itraconazole was 0.144 mu g/mL. Cross-resistance among azoles was not common (3.2%), but the parallel increase in fluconazole and itraconazole MIC has been observed (P LT 0.01). The low rate of susceptibility to fluconazole stresses the need for active antifungal surveillance of C. neoformans and of the corresponding data from different geographic regions. (C) 2012 Elsevier Masson SAS. All rights reserved.",
journal = "Journal de Mycologie Medicale",
title = "In vitro antifungal activities of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole against Cryptococcus neoformans isolated from cerebrospinal fluid and blood from patients in Serbia",
volume = "22",
number = "3",
pages = "243-248",
doi = "10.1016/j.mycmed.2012.06.002"
}
23
22
23

Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation

Isenović, Esma R.; Kedees, Mamdouh H.; Haidara, Mohamed A.; Trpković, Andreja; Mikhailidis, Dimitri P.; Marche, Pierre

(2010)

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Kedees, Mamdouh H.
AU  - Haidara, Mohamed A.
AU  - Trpković, Andreja
AU  - Mikhailidis, Dimitri P.
AU  - Marche, Pierre
PY  - 2010
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3984
AB  - It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42- and 44-kDa isoforms (ERK1/2)participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS) and thrombin (Thr). However, understanding of the intracellular signal transduction pathways involved is incomplete. This review considers the recent findings in INS and Thr signaling mechanisms that modulate the proliferation of VSMCs with particular emphasis on the ERK1/2 signaling pathway, an important mediator of VSMCs hypertrophy and vascular disease. Moreover, because the ERK1/2 pathway have been acknowledged as an important mediator of VSMCs hypertrophy, ERK1/2 is identified as a key target for novel therapeutic interventions to minimize irreversible tissue damage associated with hypertension and atherosclerosis.
T2  - Angiology
T1  - Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation
VL  - 61
IS  - 4
SP  - 357
EP  - 364
DO  - 10.1177/0003319709358693
ER  - 
@article{
author = "Isenović, Esma R. and Kedees, Mamdouh H. and Haidara, Mohamed A. and Trpković, Andreja and Mikhailidis, Dimitri P. and Marche, Pierre",
year = "2010",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3984",
abstract = "It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42- and 44-kDa isoforms (ERK1/2)participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS) and thrombin (Thr). However, understanding of the intracellular signal transduction pathways involved is incomplete. This review considers the recent findings in INS and Thr signaling mechanisms that modulate the proliferation of VSMCs with particular emphasis on the ERK1/2 signaling pathway, an important mediator of VSMCs hypertrophy and vascular disease. Moreover, because the ERK1/2 pathway have been acknowledged as an important mediator of VSMCs hypertrophy, ERK1/2 is identified as a key target for novel therapeutic interventions to minimize irreversible tissue damage associated with hypertension and atherosclerosis.",
journal = "Angiology",
title = "Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation",
volume = "61",
number = "4",
pages = "357-364",
doi = "10.1177/0003319709358693"
}
20
20
20

Chronic Hepatitis C, Insulin Resistance and Vascular Disease

Trpković, Andreja; Stokić, Edita; Radak, Đorđe J.; Gluvić, Zoran; Haidara, Mohamed A.; Mikhailidis, Dimitri P.; Isenović, Esma R.

(2010)

@article{
author = "Trpković, Andreja and Stokić, Edita and Radak, Đorđe J. and Gluvić, Zoran and Haidara, Mohamed A. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2010",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4208",
abstract = "The role of hepatitis C virus (HCV) infection in the development of vascular disease is controversial. Insulin resistance (IR) is a recognized risk factor for cardiovascular disease (CVD) and is associated with chronic hepatitis C (CHC). Thus, IR may promote atherosclerosis and vascular disease in CHC patients. HCV-associated IR may also cause hepatic steatosis and resistance to antiviral treatment. In addition, HCV may contribute a direct, proatherogenetic action on the vascular wall. This review considers the impact of IR on interferon-based therapy of HCV infection and the role of insulin-sensitizing agents on the response to antiviral treatment and prevention of IR complications, including CVD.",
journal = "Current Pharmaceutical Design",
title = "Chronic Hepatitis C, Insulin Resistance and Vascular Disease",
volume = "16",
number = "34",
pages = "3823-3829",
doi = "10.2174/138161210794455067"
}
5
3
2

Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles

Trpković, Andreja; Todorović-Marković, Biljana; Kleut, Duška; Misirkić, Maja; Janjetović, Kristina D.; Vucicevic, Ljubica; Pantovic, Aleksandar; Jovanović, Svetlana P.; Dramićanin, Miroslav; Marković, Zoran M.; Trajković, Vladimir S.

(2010)

TY  - JOUR
AU  - Trpković, Andreja
AU  - Todorović-Marković, Biljana
AU  - Kleut, Duška
AU  - Misirkić, Maja
AU  - Janjetović, Kristina D.
AU  - Vucicevic, Ljubica
AU  - Pantovic, Aleksandar
AU  - Jovanović, Svetlana P.
AU  - Dramićanin, Miroslav
AU  - Marković, Zoran M.
AU  - Trajković, Vladimir S.
PY  - 2010
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4093
AB  - The present study investigated the hemolytic properties of fullerene (C-60) nanoparticles prepared by solvent exchange using tetrahydrofuran (nC(60)THF), or by mechanochemically assisted complexation with macrocyclic oligosaccharide gamma-cyclodextrin (nC(60)CDX) or the copolymer ethylene vinyl acetate-ethylene vinyl versatate (nC(60)EVA-EVV). The spectrophotometrical analysis of hemoglobin release revealed that only nC(60)THF, but not nC(60)CDX or nC(60)EVA-EVV, was able to cause lysis of human erythrocytes in a dose-and time-dependent manner. Atomic force microscopy revealed that nC(60)THF-mediated hemolysis was preceded by erythrocyte shrinkage and increase in cell surface roughness. A flow cytometric analysis confirmed a decrease in erythrocyte size and demonstrated a significant increase in reactive oxygen species production in red blood cells exposed to nC(60)THF. The nC(60)THF-triggered hemolytic activity was efficiently reduced by the antioxidants N-acetylcysteine and butylated hydroxyanisole, as well as by serum albumin, the most abundant protein in human blood plasma. These data indicate that nC(60)THF can cause serum albumin-preventable hemolysis through oxidative stress-mediated damage of the erythrocyte membrane.
T2  - Nanotechnology
T1  - Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles
VL  - 21
IS  - 37
DO  - 10.1088/0957-4484/21/37/375102
ER  - 
@article{
author = "Trpković, Andreja and Todorović-Marković, Biljana and Kleut, Duška and Misirkić, Maja and Janjetović, Kristina D. and Vucicevic, Ljubica and Pantovic, Aleksandar and Jovanović, Svetlana P. and Dramićanin, Miroslav and Marković, Zoran M. and Trajković, Vladimir S.",
year = "2010",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4093",
abstract = "The present study investigated the hemolytic properties of fullerene (C-60) nanoparticles prepared by solvent exchange using tetrahydrofuran (nC(60)THF), or by mechanochemically assisted complexation with macrocyclic oligosaccharide gamma-cyclodextrin (nC(60)CDX) or the copolymer ethylene vinyl acetate-ethylene vinyl versatate (nC(60)EVA-EVV). The spectrophotometrical analysis of hemoglobin release revealed that only nC(60)THF, but not nC(60)CDX or nC(60)EVA-EVV, was able to cause lysis of human erythrocytes in a dose-and time-dependent manner. Atomic force microscopy revealed that nC(60)THF-mediated hemolysis was preceded by erythrocyte shrinkage and increase in cell surface roughness. A flow cytometric analysis confirmed a decrease in erythrocyte size and demonstrated a significant increase in reactive oxygen species production in red blood cells exposed to nC(60)THF. The nC(60)THF-triggered hemolytic activity was efficiently reduced by the antioxidants N-acetylcysteine and butylated hydroxyanisole, as well as by serum albumin, the most abundant protein in human blood plasma. These data indicate that nC(60)THF can cause serum albumin-preventable hemolysis through oxidative stress-mediated damage of the erythrocyte membrane.",
journal = "Nanotechnology",
title = "Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles",
volume = "21",
number = "37",
doi = "10.1088/0957-4484/21/37/375102"
}
27
24
27

Insulin, Thrombin, ERK1/2 Kinase and Vascular Smooth Muscle Cells Proliferation

Isenović, Esma R.; Soskić, Sanja S.; Trpković, Andreja; Dobutovic, Branislava; Popović, Milan; Gluvić, Zoran; Putnikovic, Biljana; Marche, Pierre

(2010)

@article{
author = "Isenović, Esma R. and Soskić, Sanja S. and Trpković, Andreja and Dobutovic, Branislava and Popović, Milan and Gluvić, Zoran and Putnikovic, Biljana and Marche, Pierre",
year = "2010",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4209",
abstract = "Vascular smooth muscle cells (VSMC) respond to arterial wall injury by intimal proliferation and play a key role in atherogenesis by proliferating and migrating excessively in response to repeated injury, such as hypertension and atherosclerosis. In contrast, fully differentiated, quiescent VSMC allow arterial vasodilatation and vasoconstriction. Exaggerated and uncontrolled VSMC proliferation appears therefore to be a common feature of both atherosclerosis and hypertension. Signal transduction pathways in eukaryotic cells integrate diverse extracellular signals, and regulate complex biological responses such as growth, differentiation and death. One group of proline-directed Ser/Thr protein kinases, the mitogen-activated protein kinases (MAPKs), plays a central role in these signalling pathways. Much attention has focused in recent years on subfamilies of MAPKs, the extracellular signal regulated kinases (ERKs). Here we overview the work on ERKs 1 to 2, emphasising when possible their biological activities in VSMC proliferation. It is clear from numerosus studies including our own, that ERK1/ERK2 pathway has an imoprtant role in VSMC proliferation induced by insulin (INS) and thrombin. Despite the physiological and pathophysiological importance of INS and thrombin, possible signal transduction pathways involved in INS and thrombin regulation of VSMCs proliferation remains poorly understood. Thus, this review examines recent findings in signalling mechanisms involved in INS and thrombin-triggered VSMCs proliferation with particular emphasis on ERK1/2 signalling pathways. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review.",
journal = "Current Pharmaceutical Design",
title = "Insulin, Thrombin, ERK1/2 Kinase and Vascular Smooth Muscle Cells Proliferation",
volume = "16",
number = "35",
pages = "3895-3902",
doi = "10.2174/138161210794454987"
}
18
19
21

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

Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation

Isenović, Esma R.; Kedees, Mamdouh H.; Tepavčević, Snežana; Milosavljević, Tijana; Korićanac, Goran; Trpković, Andreja; Marche, Pierre

(2009)

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Kedees, Mamdouh H.
AU  - Tepavčević, Snežana
AU  - Milosavljević, Tijana
AU  - Korićanac, Goran
AU  - Trpković, Andreja
AU  - Marche, Pierre
PY  - 2009
UR  - http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1871-529X&volume=9&issue=3&spage=172
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7802
AB  - Vascular smooth muscle cells (VSMCs) respond to arterial wall injury by intimal proliferation and play a key role in atherogenesis by proliferating and migrating excessively in response to repeated injury, such as hypertension and atherosclerosis. In contrast, fully differentiated, quiescent VSMCs allow arterial vasodilatation and vasoconstriction. Exaggerated and uncontrolled VSMCs proliferation appears therefore to be a common feature of both atherosclerosis and hypertension. Phosphorylation/dephosphorylation reactions of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) as well as Akt and cytosolic phospholipase 2 (cPLA 2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS). The ability of INS to significantly increase VSMCs proliferation has been demonstrated in several systems, but understanding of the intracellular signal transduction pathways involved is incomplete. Signal transduction pathways involved in regulation of the VSMCs proliferation by INS remains poorly understood. Thus, this review examines recent findings in signaling mechanisms employed by INS in modulating the regulation of proliferation of VSMCs with particular emphasis on PI3K/Akt, cPLA2 and ERK1/2 signaling pathways that have been identified as important mediators of VSMCs hypertrophy and vascular diseases. These findings are critical for understanding the role of INS in vascular biology and hyperinsulinemia.
T2  - Cardiovascular & Hematological Disorders-Drug Targets
T1  - Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation
VL  - 9
IS  - 3
SP  - 172
EP  - 180
DO  - 10.2174/187152909789007034
ER  - 
@article{
author = "Isenović, Esma R. and Kedees, Mamdouh H. and Tepavčević, Snežana and Milosavljević, Tijana and Korićanac, Goran and Trpković, Andreja and Marche, Pierre",
year = "2009",
url = "http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1871-529X&volume=9&issue=3&spage=172, http://vinar.vin.bg.ac.rs/handle/123456789/7802",
abstract = "Vascular smooth muscle cells (VSMCs) respond to arterial wall injury by intimal proliferation and play a key role in atherogenesis by proliferating and migrating excessively in response to repeated injury, such as hypertension and atherosclerosis. In contrast, fully differentiated, quiescent VSMCs allow arterial vasodilatation and vasoconstriction. Exaggerated and uncontrolled VSMCs proliferation appears therefore to be a common feature of both atherosclerosis and hypertension. Phosphorylation/dephosphorylation reactions of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) as well as Akt and cytosolic phospholipase 2 (cPLA 2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS). The ability of INS to significantly increase VSMCs proliferation has been demonstrated in several systems, but understanding of the intracellular signal transduction pathways involved is incomplete. Signal transduction pathways involved in regulation of the VSMCs proliferation by INS remains poorly understood. Thus, this review examines recent findings in signaling mechanisms employed by INS in modulating the regulation of proliferation of VSMCs with particular emphasis on PI3K/Akt, cPLA2 and ERK1/2 signaling pathways that have been identified as important mediators of VSMCs hypertrophy and vascular diseases. These findings are critical for understanding the role of INS in vascular biology and hyperinsulinemia.",
journal = "Cardiovascular & Hematological Disorders-Drug Targets",
title = "Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation",
volume = "9",
number = "3",
pages = "172-180",
doi = "10.2174/187152909789007034"
}
30
33

Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation

Isenović, Esma R.; Kedees, Mamdouh H.; Tepavčević, Snežana; Milosavljević, Tijana; Korićanac, Goran; Trpković, Andreja; Marche, Pierre

(2009)

@article{
author = "Isenović, Esma R. and Kedees, Mamdouh H. and Tepavčević, Snežana and Milosavljević, Tijana and Korićanac, Goran and Trpković, Andreja and Marche, Pierre",
year = "2009",
url = "http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1871-529X&volume=9&issue=3&spage=172, http://vinar.vin.bg.ac.rs/handle/123456789/7832",
abstract = "Vascular smooth muscle cells (VSMCs) respond to arterial wall injury by intimal proliferation and play a key role in atherogenesis by proliferating and migrating excessively in response to repeated injury, such as hypertension and atherosclerosis. In contrast, fully differentiated, quiescent VSMCs allow arterial vasodilatation and vasoconstriction. Exaggerated and uncontrolled VSMCs proliferation appears therefore to be a common feature of both atherosclerosis and hypertension. Phosphorylation/dephosphorylation reactions of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) as well as Akt and cytosolic phospholipase 2 (cPLA 2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS). The ability of INS to significantly increase VSMCs proliferation has been demonstrated in several systems, but understanding of the intracellular signal transduction pathways involved is incomplete. Signal transduction pathways involved in regulation of the VSMCs proliferation by INS remains poorly understood. Thus, this review examines recent findings in signaling mechanisms employed by INS in modulating the regulation of proliferation of VSMCs with particular emphasis on PI3K/Akt, cPLA2 and ERK1/2 signaling pathways that have been identified as important mediators of VSMCs hypertrophy and vascular diseases. These findings are critical for understanding the role of INS in vascular biology and hyperinsulinemia.",
journal = "Cardiovascular & Hematological Disorders-Drug Targets",
title = "Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation",
volume = "9",
number = "3",
pages = "172-180",
doi = "10.2174/187152909789007034"
}
30
33

Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy

Isenović, Esma R.; Trpković, Andreja; Žakula, Zorica; Korićanac, Goran; Marche, Pierre

(2008)

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Trpković, Andreja
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Marche, Pierre
PY  - 2008
UR  - http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4021&volume=4&issue=3&spage=190
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7803
AB  - It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review.
T2  - Current Hypertension Reviews
T1  - Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy
VL  - 4
IS  - 3
SP  - 190
EP  - 196
DO  - 10.2174/157340208785132590
ER  - 
@article{
author = "Isenović, Esma R. and Trpković, Andreja and Žakula, Zorica and Korićanac, Goran and Marche, Pierre",
year = "2008",
url = "http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4021&volume=4&issue=3&spage=190, http://vinar.vin.bg.ac.rs/handle/123456789/7803",
abstract = "It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review.",
journal = "Current Hypertension Reviews",
title = "Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy",
volume = "4",
number = "3",
pages = "190-196",
doi = "10.2174/157340208785132590"
}
3
5

Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy

Isenović, Esma R.; Trpković, Andreja; Žakula, Zorica; Korićanac, Goran; Marche, Pierre

(2008)

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Trpković, Andreja
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Marche, Pierre
PY  - 2008
UR  - http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4021&volume=4&issue=3&spage=190
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7837
AB  - It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review. © 2008 Bentham Science Publishers Ltd.
T2  - Current Hypertension Reviews
T1  - Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy
VL  - 4
IS  - 3
SP  - 190
EP  - 196
DO  - 10.2174/157340208785132590
ER  - 
@article{
author = "Isenović, Esma R. and Trpković, Andreja and Žakula, Zorica and Korićanac, Goran and Marche, Pierre",
year = "2008",
url = "http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4021&volume=4&issue=3&spage=190, http://vinar.vin.bg.ac.rs/handle/123456789/7837",
abstract = "It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review. © 2008 Bentham Science Publishers Ltd.",
journal = "Current Hypertension Reviews",
title = "Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy",
volume = "4",
number = "3",
pages = "190-196",
doi = "10.2174/157340208785132590"
}
3
5