Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation
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Autori
Isenović, Esma R.Kedees, Mamdouh H.
Tepavčević, Snežana
Milosavljević, Tijana
Korićanac, Goran
Trpković, Andreja
Marche, Pierre
Prikaz (Objavljena verzija)
,
© 2009 Bentham Science Publishers Ltd
Metapodaci
Prikaz svih podataka o dokumentuApstrakt
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 activato...rs, 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.
Ključne reči:
cPLA2 / ERK1/2 / insulin / PI3K/Akt / proliferation / VSMCsIzvor:
Cardiovascular and Hematological Disorders-Drug Targets, 2009, 9, 3, 172-180
DOI: 10.2174/187152909789007034
ISSN: 1871-529X
PubMed: 19534657
Scopus: 2-s2.0-73249149543
URI
http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1871-529X&volume=9&issue=3&spage=172https://vinar.vin.bg.ac.rs/handle/123456789/7832
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VinčaTY - 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 . .