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The eIF2B-interacting domain of RGS2 protects against GPCR agonist-induced hypertrophy in neonatal rat cardiomyocytes.

Abstract：

:The protective effect of Regulator of G protein Signaling 2 (RGS2) in cardiac hypertrophy is thought to occur through its ability to inhibit the chronic GPCR signaling that promotes pathogenic growth both in vivo and in cultured cardiomyocytes. However, RGS2 is known to have additional functions beyond its activity as a GTPase accelerating protein, such as the ability to bind to eukaryotic initiation factor, eIF2B, and inhibit protein synthesis. The RGS2 eIF2B-interacting domain (RGS2(eb)) was examined for its ability to regulate hypertrophy in neonatal ventricular myocytes. Both full-length RGS2 and RGS2(eb) were able to inhibit agonist-induced cardiomyocyte hypertrophy, but RGS2(eb) had no effect on receptor-mediated inositol phosphate production, cAMP production, or ERK 1/2 activation. These results suggest that the protective effects of RGS2 in cardiac hypertrophy may derive at least in part from its ability to govern protein synthesis.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Chidiac P,Sobiesiak AJ,Lee KN,Gros R,Nguyen CH

doi

10.1016/j.cellsig.2014.02.006

subject

Has Abstract

pub_date

2014-06-01 00:00:00

pages

1226-34

issue

6

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(14)00066-7

journal_volume

26

pub_type

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