Format

Send to

Choose Destination
Biochem Biophys Res Commun. 2017 Jan 29;483(1):75-81. doi: 10.1016/j.bbrc.2017.01.003. Epub 2017 Jan 4.

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

Author information

1
Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, Brazil.
2
Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, Brazil. Electronic address: krieger@incor.usp.br.

Abstract

Recent evidence suggests that β-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 β-arrestin 1 and 2 subjected to shear stress (SS, 15 dynes/cm2, 10 min). The downregulation of β-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 β-arrestin interacts with Akt, eNOS and caveolin-1 and these interactions are not influenced by SS. Our data indicate that β-arrestins and Akt/eNOS downstream signaling are required for early SS-induced NO production in SVECs, which is consistent with the idea that β-arrestins and caveolin-1 are part of a pre-assembled complex associated with the cellular mechanotransduction machinery.

KEYWORDS:

Endothelial cells; Mechanotransduction; Nitric oxide; Shear stress; β-arrestin

PMID:
28062183
DOI:
10.1016/j.bbrc.2017.01.003
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center