AAV-mediated knock-down of HRC exacerbates transverse aorta constriction-induced heart failure.

ABSTRACT:

Background

Histidine-rich calcium binding protein (HRC) is located in the lumen of sarcoplasmic reticulum (SR) that binds to both triadin (TRN) and SERCA affecting Ca(2+) cycling in the SR. Chronic overexpression of HRC that may disrupt intracellular Ca(2+) homeostasis is implicated in pathogenesis of cardiac hypertrophy. Ablation of HRC showed relatively normal phenotypes under basal condition, but exhibited a significantly increased susceptibility to isoproterenol-induced cardiac hypertrophy. In the present study, we characterized the functions of HRC related to Ca(2+) cycling and pathogenesis of cardiac hypertrophy using the in vitro siRNA- and the in vivo adeno-associated virus (AAV)-mediated HRC knock-down (KD) systems, respectively.

Methodology/principal findings

AAV-m

SUBMITTER: Park CS 

PROVIDER: S-EPMC3429470 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature