Antiapoptotic effect of glutaredoxin in cardiomyocytes by inducing changes in the cellular redox system.

点击翻译按钮获取中文摘要

It is known that glutaredoxin (GRX) protects cells from oxidative stress by regulating the redox state of certain proteins. In GRX1-overexpressed rat myocardiac H9c2 cells (H9c2-GRX), nitric oxide (NO)-induced apoptosis and decreasing of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity was suppressed compare to H9c2-control cells (H9c2-control). Furthermore, under NO stimulation, nuclear translocation of GAPDH and S-nitrosylation of protein was suppressed in H9c2-GRX compare to H9c2-control. These data suggest that the overexpression of GRX1 could protect cardiomyocytes against NO-induced apoptosis, likely through the inhibition of the oxidative modification and the nuclear translocation of GAPDH.