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dc.creatorIsenović, Esma R.
dc.creatorTrpković, Andreja
dc.creatorŽakula, Zorica
dc.creatorKorićanac, Goran
dc.creatorMarche, Pierre
dc.date.accessioned2018-10-04T10:36:51Z
dc.date.available2018-10-04T10:36:51Z
dc.date.issued2008
dc.identifier.issn1573-4021
dc.identifier.urihttp://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4021&volume=4&issue=3&spage=190
dc.identifier.urihttp://vinar.vin.bg.ac.rs/handle/123456789/7837
dc.description.abstractIt 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.en
dc.rightsrestrictedAccess
dc.sourceCurrent Hypertension Reviews
dc.subjectCalcium-channelsen
dc.subjectEpidermal growth factor receptoren
dc.subjectERK1/2 signaling pathwayen
dc.subjectHypertrophyen
dc.subjectThrombinen
dc.subjectVascular smooth muscle cellsen
dc.titleRole of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophyen
dc.typearticleen
dc.rights.licenseARR
dcterms.abstractМарцхе, Пиерре; Корићанац, Горан; Исеновић, Есма Р.; Трпковић, Aндреја; Закула, Зорица;
dc.rights.holder© 2008 Bentham Science Publishers Ltd
dc.citation.volume4
dc.citation.issue3
dc.citation.spage190
dc.citation.epage196
dc.identifier.doi10.2174/157340208785132590
dc.type.versionpublishedVersion
dc.identifier.scopus2-s2.0-54749108385


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