Antiapoptotic effect of glutaredoxin in myocardiac cellsb induced by regulationg the redox state of GAPDH.

已知，NO诱导的GAPDH的S亚硝化可诱导其核移位，导致细胞凋亡。在H9c2对照细胞中，与GRX1过表达的大鼠心肌H9c2细胞(H9c2-GRX)相比，NO诱导的细胞死亡呈剂量依赖性增加。我们发现GRX1抑制H9c2-GRX中GAPDH的S亚硝化。此外，与H9c2对照细胞相比，H9c2-GRX细胞中NO诱导的GAPDH核转位减少。提示GRX可能通过抑制GAPDH的S亚硝化作用而发挥抗细胞凋亡作用。

It is known that NO induced S-nitrosylation of GAPDH elicits its nuclear translocation and causes apoptotic cell death. In H9c2-control cells, NO-induced cell death increased dose-dependently compare to GRX1-overexpressed rat myocardiac H9c2 cells(H9c2-GRX). We revealed that GRX1 suppressed S-nitrosylation of GAPDH in H9c2-GRX. In addition, NO-induced nuclear translocation of GAPDH was decreased in H9c2-GRX compared to H9c2 control cells. These data suggest that GRX exerts the antiapoptotic effect by suppressing the S-nitrosylation of GAPDH.