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Vasoinhibins 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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dc.creator Stéphanie Thebault
dc.creator Carmen González
dc.creator Celina García
dc.creator David Arredondo Zamarripa
dc.creator Gabriel Nava
dc.creator Luis Vaca
dc.creator Fernando López-Casillas
dc.creator Gonzalo Martínez De la Escalera
dc.creator Carmen Clapp
dc.date 2011
dc.date.accessioned 2013-05-30T12:27:31Z
dc.date.available 2013-05-30T12:27:31Z
dc.date.issued 2013-05-30
dc.identifier http://www.mdpi.com/1424-8247/4/7/1052/
dc.identifier http://www.doaj.org/doaj?func=openurl&genre=article&issn=14248247&date=2011&volume=4&issue=7&spage=1052
dc.identifier.uri http://koha.mediu.edu.my:8181/jspui/handle/123456789/5215
dc.description Vasoinhibins, 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.language eng
dc.publisher Molecular Diversity Preservation International
dc.source Pharmaceuticals
dc.subject vasoinhibins
dc.subject 16kDa-prolactin
dc.subject bradykinin
dc.subject endothelial nitric oxide synthase
dc.subject calcium mobilization
dc.subject transient receptor potential channels
dc.title Vasoinhibins 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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