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Yuan, Yang; Zheng, Yanrong; Zhang, Xiangnan; Chen, Ying; Wu, Xiaoli; Wu, Jiaying; Shen, Zhe; Jiang, Lei; Wang, Lu; Yang, Wei; Luo, Jianhong; Qin, Zhenghong; Hu, Weiwei; Chen, Zhong
Autophagy, 10/2017, Volume: 13, Issue: 10Journal Article
Cerebral ischemia induces massive mitochondrial damage. These damaged mitochondria are cleared, thus attenuating brain injury, by mitophagy. Here, we identified the involvement of BNIP3L/NIX in cerebral ischemia-reperfusion (I-R)-induced mitophagy. Bnip3l knockout (bnip3l −/− ) impaired mitophagy and aggravated cerebral I-R injury in mice, which can be rescued by BNIP3L overexpression. The rescuing effects of BNIP3L overexpression can be observed in park2 −/− mice, which showed mitophagy deficiency after I-R. Interestingly, bnip3l and park2 double-knockout mice showed a synergistic mitophagy deficiency with I-R treatment, which further highlighted the roles of BNIP3L-mediated mitophagy as being independent from PARK2. Further experiments indicated that phosphorylation of BNIP3L serine 81 is critical for BNIP3L-mediated mitophagy. Nonphosphorylatable mutant BNIP3L S81A failed to counteract both mitophagy impairment and neuroprotective effects in bnip3l −/− mice. Our findings offer insights into mitochondrial quality control in ischemic stroke and bring forth the concept that BNIP3L could be a potential therapeutic target for ischemic stroke, beyond its accepted role in reticulocyte maturation.
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