Denitrosylation of S-nitrosylated OGT is triggered in LPS-stimulated innate immune response |
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| Authors: | Ryu In-Hyun Do Su-Il |
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| Affiliation: | aDepartment of Cardiology, Peking University Third Hospital, No. 49 North Garden Road, Beijing 100191, China;bInstitute of Molecular Medicine, Peking University, No. 5 Yi He Yuan Road, Beijing 100871, China;cCardiovascular Center, University of Michigan, 1150 W Medical Center Drive, Ann Arbor, MI 48109, USA;dCardiovascular Research Institute, Morehouse School of Medicine, 720 Westview Drive SW, Atlanta, GA 30310, USA |
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| Abstract: | Rad is a member of a subclass of small GTP-binding proteins, the RGK family. In the present study we investigated the role of Rad protein in regulating cardiomyocyte viability. DNA fragmentation and TUNEL assays demonstrated that Rad promoted rat neonatal cardiomyocyte apoptosis. Rad silencing fully blocked serum deprivation induced apoptosis, indicating Rad is necessary for trigger cardiomyocyte apoptosis. Rad overexpression caused a dramatic decrease of the anti-apoptotic molecule Bcl-xL, whereas Bcl-xL overexpression protected cardiomyocytes against Rad-induced apoptosis. Rad-triggered apoptosis was mediated by the activation of p38 MAPK. The p38 blocker SB203580 effectively protected cardiomyocytes against Rad-evoked apoptosis. |
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| Keywords: | Rad GTPase Cardiomyocyte Apoptosis p38 MAPK Bcl-xL |
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