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

Autor(es)

Carneiro, Ana Paula ; Fonseca-Alaniz, Miriam Helena ; Dallan, Luis Alberto Oliveira ; Miyakawa, Ayumi Aurea ; Krieger, Jose Eduardo

• Tipo de documento: Artigo Científico
• Fonte: Biochemical and Biophysical Research Communications; v. 483, n. 1, p. 75-81, JAN 29 2017.
• Citações Web of Science: 0

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. (C) 2017 Elsevier Inc. All rights reserved. (AU)

• Processo FAPESP: 13/17368-0 - Genômica cardiovascular: mechanismos & novas terapias - CVGen mech2ther
• Beneficiário: José Eduardo Krieger
• Modalidade de apoio: Auxílio à Pesquisa - Temático