Che-1 inhibits oxygen–glucose deprivation/reoxygenation-induced neuronal apoptosis associated with inhibition of the p53-mediated proapoptotic signaling pathway. Issue 14 (26th September 2018)

• Record Type: Journal Article
• Authors: Guo, Shenglong; Chen, Ruili; Chen, Xiaoli; Xie, Zhen; Huo, Fangfang; Wu, Zhongliang
• Is Part Of: NeuroReport. Volume 29:Issue 14(2018)
• Publication Date: 2018-09-26
• Subjects: Che-1 -- oxygen–glucose deprivation and reoxygenation -- p53; Neurosciences -- Periodicals; Nervous system -- Periodicals; Neurophysiology -- Periodicals; Nervous System Diseases -- Periodicals; Nervous System Physiological Phenomena -- Periodicals; Neurosciences -- Periodicals; 616.805
• DOI: 10.1097/WNR.0000000000001095
• Languages: English
• ISSNs: 0959-4965

Abstract

Abstract : Accumulating evidence suggests that Che-1 is a strong antiapoptotic protein and can protect cells against various insults. However, whether Che-1 is involved in the protection of neurons against cerebral ischemia/reperfusion injury remains unclear. In this study, we aimed to investigate the potential role of Che-1 in regulating cerebral ischemia/reperfusion injury-induced neuronal injury using the oxygen–glucose deprivation and reoxygenation (OGD/R) model in vitro . We found that Che-1 expression was induced in neurons following OGD/R treatment. Functional experiments showed that Che-1 knockdown aggravated OGD/R-induced neuronal apoptosis. In contrast, Che-1 overexpression exerted a protective effect against OGD/R-induced neuronal apoptosis. Moreover, our results showed that the protective effect of Che-1 was associated with the inhibition of p53-mediated proapoptotic genes, including Puma, Noxa, and Bax. In addition, we showed that Che-1 impeded the transcript activity of p53 toward apoptosis. Taken together, our results indicate that Che-1 alleviates OGD/R-induced neuronal apoptosis in-vitro through inhibition of p53-mediated proapoptotic signaling. Our study suggests that Che-1 may serve as a potential therapeutic target for the treatment of cerebral ischemic/reperfusion injury in vivo .