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

• Project/Area Number: 21890193
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Anesthesiology/Resuscitation studies
• Research Institution: Nagasaki University
• Principal Investigator: INADOMI Chiaki 長崎大学, 大学病院, 助教 (20508444)
• Project Period (FY): 2009 – 2010
• Project Status: Completed (Fiscal Year 2010)
• Budget Amount: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000); Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000); Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
• Keywords: 酸化ストレス / 心筋保護 / 循環器・高血圧

Research Abstract

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.