Cyclosporin A inhibits cell death of cornel endothelial cells by protecting mitochondrial membrane potential

Research Project

Project/Area Number	23792005
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Ophthalmology
Research Institution	Juntendo University
Principal Investigator	FUNAKI TOSHINARI 順天堂大学, 医学部, 准教授 (80384121)
Project Period (FY)	2011 – 2013
Project Status	Completed (Fiscal Year 2013)
Budget Amount *help	¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000) Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000) Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000) Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Keywords	角膜内皮細胞 / 角膜移植 / 細胞死 / シクロスポリン / ミトコンドリア / 角膜移植術 / 膜電位
Research Abstract	We corfirmed H2O2 induced a dose dependent increase in cell death of cultured human corneal endotehelial cells(HCECs). At concentration of 100nM, Cyclosporine A(CsA) attenuated the H2O2-induced cell death of HCECs by 15%.CsA significantly inhibited the permiability trasition pore(PTP) in H2O2 treaed HCECs. The mitochondrial membrane potential of H2O2 treated mouse corneal cup were protected by CsA at concetration of 100nM. Cyclosporine A protected mitochondrial menmbrane potential from oxidative stress, abd attenuated cell death of corneal endothelial cells.

Report

(4 results)