Oxidative posttranslational modifications mediate decreased SERCA activity and myocyte dysfunction in Galphaq-overexpressing mice.

ABSTRACT:

Background

Myocyte contractile dysfunction occurs in pathological remodeling in association with abnormalities in calcium regulation. Mice with cardiac myocyte-specific overexpression of Galphaq develop progressive left ventricular failure associated with myocyte contractile dysfunction and calcium dysregulation.

Objective

We tested the hypothesis that myocyte contractile dysfunction in the Galphaq mouse heart is mediated by reactive oxygen species, and in particular, oxidative posttranslational modifications, which impair the function of sarcoplasmic reticulum Ca2+-ATPase (SERCA).

Methods and results

Freshly isolated ventricular myocytes from Galphaq mice had marked abnormalities of myocyte contractile function and calcium transients. In Galphaq myocardium, SERCA pro

SUBMITTER: Lancel S 

PROVIDER: S-EPMC2909347 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature