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

Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, Brazil.
Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, Brazil. Electronic address:


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.


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

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center