Weiqian Chen
Soochow University, China
Title: Follistatin-like 1 protects cardiomyoblasts from injury induced by sodium nitroprusside through akt/gsk-3B activation and bmp/smad1/5/9 inhibition
Biography
Biography: Weiqian Chen
Abstract
Cardiac cell apoptosis provoked by excessive sodium nitroprusside (SNP) toxicity, a potent vasodilator, limited its clinical application. Effective means for protection against SNP-induced cardiotoxicity would be highly needed. This study investigated the effects of Follistatin-like 1 (FSTL1) on the injury induced by SNP in rat cardiomyoblast H9c2 cells. SNP challenge significantly increased cardiac cell death, which was attenuated by FSTL1 pretreatment. Additionally, knockdown of endogenous FSTL1 enhanced SNP-induced cell apoptosis. Furthermore, FSTL1 pretreatment partially inhibited SNP-induced NO generation. LY294002 and BMP4 completely abolished cytoprotective role of FSTL1 against SNP challenge, indicating activation of Akt/GSK-3β and inhibition of BMP/Smad1/5/9 signaling is involved in this cellular process. Lastly, FSTL1-mediated cytoprotection is independent of Smad2/3 signaling, as SB525334 failed to remove its protective role. Taken together, these results indicated that FSTL1 protected the SNP-induced injury in cardiac H9c2 cells through, at least in part, the activation of Akt/GSK-3β and inhibition of Smad1/5/9 signaling.