Overexpression of PEP-19 Suppresses Angiotensin II-Induced Cardiomyocyte Hypertrophy

• Main Authors: Yang-yang Xie (Author), Meng-meng Sun (Author), Xue-fang Lou (Author), Chen Zhang (Author), Feng Han (Author), Bo-ya Zhang (Author), Ping Wang (Author), Ying-mei Lu (Author)
• Format: Book
• Published: Elsevier, 2014-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

Abstract.: The precise molecular mechanisms leading to disturbance of Ca2+/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. Keywords:: angiotensin II, calmodulin kinase II, calcineurin, PEP-19, cardiomyocyte hypertrophy

Item Description

1347-8613
10.1254/jphs.13208FP