beta-arrestin is critical for early shear stress-induced Akt/eNOS activation in human vascular endothelial cells

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art_CARNEIRO_betaarrestin_is_critical_for_early_shear_stressinduced_AkteNOS_2017.PDF (1.16 MB)
Citações na Scopus
10
Tipo de produção
article
Data de publicação
2017
Editora
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI
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Scopus
Web of Science
PubMed
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Citação
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.483, n.1, p.75-81, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Recent evidence suggests that beta-arrestins, which are involved in G protein-coupled receptors desensitization, may influence mechanotransduction. Here, we observed that nitric oxide (NO) production was abrogated in human saphenous vein endothelial cells (SVECs) transfected with siRNA against beta-arrestin 1 and 2 subjected to shear stress (SS, 15 dynes/cm2, 10 min). The downregulation of beta-arrestins 1/2 in SVECs cells also prevented the SS-induced rise in levels of phosphorylation of Akt and endothelial nitric oxide synthase (eNOS, Serine 1177). Interestingly, immunoprecipitation revealed that beta-arrestin interacts with Akt, eNOS and caveolin-1 and these interactions are not influenced by SS. Our data indicate that barrestins and Akt/eNOS downstream signaling are required for early SS-induced NO production in SVECs, which is consistent with the idea that beta-arrestins and caveolin-1 are part of a pre-assembled complex associated with the cellular mechanotransduction machinery.
Palavras-chave
beta-arrestin, Mechanotransduction, Shear stress, Nitric oxide, Endothelial cells
URI
https://observatorio.fm.usp.br/handle/OPI/18790
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Coleções
Artigos e Materiais de Revistas Científicas - FM/MCP
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/11
Artigos e Materiais de Revistas Científicas - LIM/13
Artigos e Materiais de Revistas Científicas - ODS/03