TP53-induced glycolysis and apoptosis regulator is indispensable for mitochondria quality control and degradation following damage

TP53 诱导的糖酵解和凋亡调节剂对于线粒体质量控制和损伤后的降解至关重要

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作者:Jing Feng, Li Luo, Yong Liu, Shaozhi Fu, Jie Chen, Xiaoxia Duan, Li Xiang, Yanling Zhang, Jinbo Wu, Juan Fan, Qinglian Wen, Ye Zhang, Jingpin Yang, Jinxia Peng, Ming Zhao, Linglin Yang

Abstract

Mitochondria have been described as 'the powerhouse of the cell' as the organelle generates the majority of adenosine triphosphate (ATP) in cells to support life. Mitochondria can be damaged due to stress, for example by reactive oxygen species (ROS). TP53-induced glycolysis and apoptosis regulator (TIGAR) serves a role in suppressing ROS damage and may protect mitochondria integrity. In the present study, the localization of TIGAR on mitochondria in 5-8F cells was demonstrated. Furthermore, it was indicated that the knockdown of TIGAR using lentivirus-short hairpin RNA induces the loss of mitochondrial membrane potential and cytochrome c leakage. However, these damaged mitochondria were not degraded in cells, but exhibited an abnormal appearance as indicated by mitochondrial swelling, crista collapse and vacuolization, with physiological dysfunction marked by reduced ATP production. Therefore, TIGAR maybe an indispensable protein for mitochondrial protection and degradation following cellular damage.

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