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  - https://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",
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"
}

Isenović, E. R., Kedees, M. H., Haidara, M. A., Trpković, A., Mikhailidis, D. P.,& Marche, P.. (2010). Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation. in Angiology, 61(4), 357-364.
https://doi.org/10.1177/0003319709358693

Isenović ER, Kedees MH, Haidara MA, Trpković A, Mikhailidis DP, Marche P. Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation. in Angiology. 2010;61(4):357-364.
doi:10.1177/0003319709358693 .

Isenović, Esma R., Kedees, Mamdouh H., Haidara, Mohamed A., Trpković, Andreja, Mikhailidis, Dimitri P., Marche, Pierre, "Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation" in Angiology, 61, no. 4 (2010):357-364,
https://doi.org/10.1177/0003319709358693 . .

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  - https://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 and 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",
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 and 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"
}

Isenović, E. R., Kedees, M. H., Tepavčević, S., Milosavljević, T., Korićanac, G., Trpković, A.,& Marche, P.. (2009). Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation. in Cardiovascular and Hematological Disorders-Drug Targets, 9(3), 172-180.
https://doi.org/10.2174/187152909789007034

Isenović ER, Kedees MH, Tepavčević S, Milosavljević T, Korićanac G, Trpković A, Marche P. Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation. in Cardiovascular and Hematological Disorders-Drug Targets. 2009;9(3):172-180.
doi:10.2174/187152909789007034 .

Isenović, Esma R., Kedees, Mamdouh H., Tepavčević, Snežana, Milosavljević, Tijana, Korićanac, Goran, Trpković, Andreja, Marche, Pierre, "Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation" in Cardiovascular and Hematological Disorders-Drug Targets, 9, no. 3 (2009):172-180,
https://doi.org/10.2174/187152909789007034 . .

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  - https://vinar.vin.bg.ac.rs/handle/123456789/7832
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 and 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",
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 and 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"
}

Isenović, E. R., Kedees, M. H., Tepavčević, S., Milosavljević, T., Korićanac, G., Trpković, A.,& Marche, P.. (2009). Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation. in Cardiovascular and Hematological Disorders-Drug Targets, 9(3), 172-180.
https://doi.org/10.2174/187152909789007034

Isenović ER, Kedees MH, Tepavčević S, Milosavljević T, Korićanac G, Trpković A, Marche P. Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation. in Cardiovascular and Hematological Disorders-Drug Targets. 2009;9(3):172-180.
doi:10.2174/187152909789007034 .

Isenović, Esma R., Kedees, Mamdouh H., Tepavčević, Snežana, Milosavljević, Tijana, Korićanac, Goran, Trpković, Andreja, Marche, Pierre, "Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation" in Cardiovascular and Hematological Disorders-Drug Targets, 9, no. 3 (2009):172-180,
https://doi.org/10.2174/187152909789007034 . .