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Please use this identifier to cite or link to this item: http://dspace.mediu.edu.my:8181/xmlui/handle/123456789/5215
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dc.creatorStéphanie Thebault-
dc.creatorCarmen González-
dc.creatorCelina García-
dc.creatorDavid Arredondo Zamarripa-
dc.creatorGabriel Nava-
dc.creatorLuis Vaca-
dc.creatorFernando López-Casillas-
dc.creatorGonzalo Martínez De la Escalera-
dc.creatorCarmen Clapp-
dc.date2011-
dc.date.accessioned2013-05-30T12:27:31Z-
dc.date.available2013-05-30T12:27:31Z-
dc.date.issued2013-05-30-
dc.identifierhttp://www.mdpi.com/1424-8247/4/7/1052/-
dc.identifierhttp://www.doaj.org/doaj?func=openurl&genre=article&issn=14248247&date=2011&volume=4&issue=7&spage=1052-
dc.identifier.urihttp://koha.mediu.edu.my:8181/jspui/handle/123456789/5215-
dc.descriptionVasoinhibins, a family of antiangiogenic peptides derived from prolactin proteolysis, inhibit the vascular effects of several proangiogenic factors, including bradykinin (BK). Here, we report that vasoinhibins block the BK-induced proliferation of bovine umbilical vein endothelial cells. This effect is mediated by the inactivation of endothelial nitric oxide synthase (eNOS), as the NO donor DETA-NONOate reverted vasoinhibin action. It is an experimentally proven fact that the elevation of intracellular Ca2+ levels ([Ca2+]i) upon BK stimulation activates eNOS, and vasoinhibins blocked the BK-mediated activation of phospholipase C and the formation of inositol 1,4,5-triphosphate leading to a reduced release of Ca2+ from intracellular stores. The [Ca2+]i rise evoked by BK also involves the influx of extracellular Ca2+ via canonical transient receptor potential (TRPC) channels. Vasoinhibins likely interfere with TRPC-mediated Ca2+ entry since La3+, which is an enhancer of TRPC4 and TRPC5 channel activity, prevented vasoinhibins from blocking the stimulation by BK of endothelial cell NO production and proliferation, and vasoinhibins reduced the BK-induced increase of TRPC5 mRNA expression. Finally, vasoinhibins prevented the BK-induced phosphorylation of eNOS at Ser1179, a post-translational modification that facilitates Ca2+-calmodulin activation of eNOS. Together, our data show that vasoinhibins, by lowering NO production through the inhibition of both [Ca2+]i mobilization and eNOS phosphorylation, prevent the BK-induced stimulation of endothelial cell proliferation. Thus, vasoinhibins help to regulate BK effects on angiogenesis and vascular homeostasis.-
dc.languageeng-
dc.publisherMolecular Diversity Preservation International-
dc.sourcePharmaceuticals-
dc.subjectvasoinhibins-
dc.subject16kDa-prolactin-
dc.subjectbradykinin-
dc.subjectendothelial nitric oxide synthase-
dc.subjectcalcium mobilization-
dc.subjecttransient receptor potential channels-
dc.titleVasoinhibins Prevent Bradykinin-Stimulated Endothelial Cell Proliferation by Inactivating eNOS via Reduction of both Intracellular Ca2+ Levels and eNOS Phosphorylation at Ser1179-
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