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

Research Project

Project/Area Number	23791715
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
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)	2011 – 2013
Project Status	Completed (Fiscal Year 2013)
Budget Amount *help	¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000) Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000) Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000) Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywords	酸化ストレス / 心筋保護 / 循環器・高血圧
Research Abstract	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.

Report

(4 results)