Overexpression of PEP-19 suppresses angiotensin II-induced cardiomyocyte hypertrophy

The precise molecular mechanisms leading to disturbance of ca 2+/calmodulin-dependent intracellular signalling in cardiac hypertrophy remains unclear. as an endogenous calmodulin regulator protein,the pathophysiology role of pep-19 during cardiac hypertrophy was investigated in the present study. we here demonstrated that pep-19 protein levels are significantly elevated in the aortic banding model in vivo and angiotensin ii-induced cardiomyocyte hypertrophy in vitro. consistent with inhibitory actions of pep-19 on cardiomyocyte hypertrophy,induction of camkii and calcineurin activation as well as hypertrophy-related genes including atrial natriuretic peptide (anp) and brain natriuretic peptide (bnp) was significantly inhibited by pep-19 transfection. moreover,pep-19 partially ameliorates angiotensin ii-induced elevation of phospho-phospholamban (thr-17) and sarcoplasmic reticulum ca2+ release in cardiomyocytes. together,our results suggest that pep-19 attenuates angiotensin ii-induced cardiomyocyte hypertrophy via suppressing the disturbance of camkii and calcineurin signaling. © the japanese pharmacological society.