Sirtuin7 is involved in protecting neurons against oxygen‐glucose deprivation and reoxygenation‐induced injury through regulation of the p53 signaling pathway

• Published in: Journal of biochemical and molecular toxicology Vol. 31; no. 10
• Main Authors: Lv, Jianrui, Tian, Junbin, Zheng, Guoxi, Zhao, Jing
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.10.2017
• Subjects: Animals; Apoptosis; Cell Line; Deprivation; Gene Knockdown Techniques; Glucose; Glucose - metabolism; Injuries; Ischemia; Mice; neuron; Neurons; Neurons - metabolism; Neurons - pathology; Oxygen; Oxygen - metabolism; oxygen‐glucose deprivation and reoxygenation; p53; p53 Protein; Reperfusion; Reperfusion Injury - genetics; Reperfusion Injury - metabolism; Reperfusion Injury - pathology; Reperfusion Injury - prevention & control; Signal Transduction; SIRT7; Sirtuins - genetics; Sirtuins - metabolism; Transcription; Tumor Suppressor Protein p53 - genetics; Tumor Suppressor Protein p53 - metabolism; neuron; oxygen-glucose deprivation and reoxygenation; SIRT7; p53
• ISSN: 1095-6670; 1099-0461
• DOI: 10.1002/jbt.21955

Sirtuin7 (SIRT7) is known to regulate apoptosis and stress responses. So far, very little is known about the role of SIRT7 in cerebral ischemia/reperfusion injury. In this study, we aimed to investigate the potential role of SIRT7 in regulating oxygen‐glucose deprivation and reoxygenation (OGD/R)‐induced injury in neurons. We found a significant increase of SIRT7 expression in neurons in response to OGD/R treatment. Knockdown of SIRT7 aggravated OGD/R‐induced injury. Knockdown of SIRT7 augmented the levels of total and acetylated p53 protein. Moreover, knockdown of SIRT7 markedly increased the transcriptional activity of p53 toward apoptosis and activated the p53‐mediated proapoptotic signaling pathway. By contrast, overexpression of SIRT7 showed the opposite effects. Taken together, the results of our study suggest that SIRT7 is involved in protecting neurons against OGD/R‐induced injury, possibly through regulation of the p53‐mediated proapoptotic signaling pathway, indicating a potential therapeutic target for cerebral ischemia/reperfusion injury.