Differential effects of S100 proteins A2 and A6 on cardiac Ca(2+) cycling and contractile performance.

ABSTRACT: Defective intracellular calcium (Ca(2+)) handling is implicated in the pathogenesis of heart failure. Novel approaches targeting both cardiac Ca(2+) release and reuptake processes, such as S100A1, have the potential to rescue the function of failing cardiac myocytes. Here, we show that two members of the S100 Ca(2+) binding protein family, S100A2 and S100A6 that share high sequence homology, differentially influence cardiac Ca(2+) handling and contractility. Cardiac gene expression of S100A2 significantly enhanced both contractile and relaxation performance of rodent and canine cardiac myocytes, mimicking the functional effects of its cardiac homologue, S100A1. To interrogate mechanism, Ca(2+) spark frequency, a measure of the gating of the ryanodine receptor Ca(2+) release channel, was fo

SUBMITTER: Wang W 

PROVIDER: S-EPMC4041381 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature