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dc.contributor German Research Foundation:Collaborative Research Center 834 Wang SP Iring, András Strilic B Juarez JA Kaur H 2015-11-29T21:24:55Z 2015-11-29T21:24:55Z 2015
dc.identifier.citation pagination=3077-3086;journalVolume=125;journalIssueNumber=8;journalTitle=JOURNAL OF CLINICAL INVESTIGATION; hu
dc.identifier.uri doi:10.1172/JCI81067
dc.description.abstract Elevated blood pressure is a key risk factor for developing cardiovascular diseases. Blood pressure is largely determined by vasodilatory mediators, such as nitric oxide (NO), that are released from the endothelium in response to fluid shear stress exerted by the flowing blood. Previous work has identified several mechanotransduction signaling processes that are involved in fluid shear stress induced endothelial effects, but how fluid shear stress initiates the response is poorly understood. Here, we evaluated human and bovine endothelial cells and found that the purinergic receptor P2Y(2) and the G proteins G(q)/G(11) mediate fluid shear stress induced endothelial responses, including [Ca2+](i) transients, activation of the endothelial NO synthase (eNOS), phosphorylation of PECAM-1 and VEGFR-2, as well as activation of SRC and Ala. In response to fluid shear stress, endothelial cells released ATP, which activates the purinergic P2Y2 receptor. Mice with induced endothelium-specific P2Y(2) or G(q)/G(11) deficiency lacked flow-induced vasodilation and developed hypertension that was accompanied by reduced eNOS activation. Together, our data identify P2Y(2) and G(q)/G(11), as a critical endothelial mechanosignaling pathway that is upstream of previously described mechanotransduction processes and demonstrate that P2Y(2) and G(q)/G(11) are required for basal endothelial NO formation, vascular tone, and blood pressure. hu
dc.relation.ispartof urn:issn:0021-9738
dc.title P2Y(2) and G(q)/G(11) control blood pressure by mediating endothelial mechanotransduction hu
dc.type Journal Article hu 2015-11-29T21:21:27Z
dc.language.rfc3066 en hu
dc.identifier.mtmt 2951155
dc.identifier.wos 000359034800019
dc.identifier.pubmed 26168216
dc.contributor.department SE/AOK/I/Klinikai Kísérleti Kutató- és Humán Élettani Intézet
dc.contributor.institution Semmelweis Egyetem

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