Gelsolin (GSN) induces cardiomyocyte hypertrophy and BNP expression via p38 signaling and GATA-4 transcriptional factor

Cardiomyocyte hypertrophy is an adaptive response of the heart to various types of stress. During the period of stress accumulation, the transition from physio- logical hypertrophy to pathological hypertrophy results in the promotion of heart failure. Gelsolin (GSN) is a member of the actin-binding proteins, which regulate dynamic actin filament organization by severing and capping. Moreover, GSN also regulates cell morphology, differentiation, movement, and apoptosis. In this study, we used H9c2 and H9c2-GSN stable clones in an attempt to understand the mechanisms of GSN overexpression in cardiomyocytes. These data showed that the overexpression of GSN in H9c2- induced cardiac hypertrophy and increased the pathological hypertrophy markers atrial natriuretic peptide brain natri- uretic peptide. Furthermore, we found that E-cadherin expression decreased with the overexpression of GSN in H9c2, but b-catenin expression increased. These data pre- sume that the cytoskeleton is loose. Further, previous studies show that the mitogen-activated protein kinase pathway can induce cardiac hypertrophy. Our data showed that p-p38 expression increased with the overexpression of GSN in H9c2, and the transcription factor p-GATA4 expression also increased, suggesting that the overexpression of GSN in H9c2-induced cardiac hypertrophy seemed to be regulated