Balancing functions of annexin A6 maintain equilibrium between hypertrophy and apoptosis in cardiomyocytes.

ABSTRACT: Pathological cardiac hypertrophy is a major risk factor associated with heart failure, a state concomitant with increased cell death. However, the mechanism governing progression of hypertrophy to apoptosis at the single-cell level remains elusive. Here, we demonstrate annexin A6 (Anxa6), a calcium (Ca(2+))-dependent phospholipid-binding protein critically regulates the transition of chronic hypertrophied cardiomyocytes to apoptosis. Treatment of the H9c2(2-1) cardiomyocytes with hypertrophic agonists upregulates and relocalizes Anxa6 with increased cytosolic punctate appearance. Live cell imaging revealed that chronic exposure to hypertrophic agonists such as phenylephrine (PE) compromises the mitochondrial membrane potential (ΔΨm) and morphological dynamics. Such chronic hypertrophic ind

SUBMITTER: Banerjee P 

PROVIDER: S-EPMC4650436 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature