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ShanghaiTech University Knowledge Management System
Cardiolipin-Dependent Mitophagy Guides Outcome after Traumatic Brain Injury | |
2019-03-06 | |
发表期刊 | JOURNAL OF NEUROSCIENCE (IF:4.4[JCR-2023],5.3[5-Year]) |
ISSN | 0270-6474 |
卷号 | 39期号:10页码:1930-1943 |
发表状态 | 已发表 |
DOI | 10.1523/JNEUROSCI.3415-17.2018 |
摘要 | Mitochondrial energy production is essential for normal brain function. Traumatic brain injury (TBI) increases brain energy demands, results in the activation of mitochondrial respiration, associated with enhanced generation of reactive oxygen species. This chain of events triggers neuronal apoptosis via oxidation of a mitochondria-specific phospholipid, cardiolipin (CL). One pathway through which cells can avoid apoptosis is via elimination of damaged mitochondria by mitophagy. Previously, we showed that externalization of CL to the mitochondrial surface acts as an elimination signal in cells. Whether CL-mediated mitophagy occurs in vivo or its significance in the disease processes are not known. In this study, we showed that TBI leads to increased mitophagy in the human brain, which was also detected using TBI models in male rats. Knockdown of CL synthase, responsible for de novo synthesis of CL, or phospholipid scramblase-3, responsible for CL translocat ion to the outer mitochondrial membrane, significantly decreased TBI-induced mitophagy. Inhibition of mitochondrial clearance by 3-methyladenine, mdivi-1, or phospholipid scramblase-3 knockdown after TBI led to a worse outcome, suggesting that mitophagy is beneficial. Together, our findings indicate that TBI-induced mitophagy is an endogenous neuroprotective process that is directed by CL, which marks damaged mitochondria for elimination, thereby limiting neuronal death and behavioral deficits. |
关键词 | apoptosis autophagy cardiolipin mitophagy neuroprotection phospholipid |
收录类别 | SCI ; SCIE |
语种 | 英语 |
资助项目 | Jiangsu Province's Natural Science Foundation[BK20160047] ; Jiangsu Province's Natural Science Foundation[BK20160044] |
WOS研究方向 | Neurosciences & Neurology |
WOS类目 | Neurosciences |
WOS记录号 | WOS:000460403400014 |
出版者 | SOC NEUROSCIENCE |
WOS关键词 | DYNAMIN-RELATED PROTEIN-1 ; AUTOPHAGIC CELL-DEATH ; PHOSPHOLIPID SCRAMBLASE-3 ; MITOCHONDRIAL FISSION ; PATHWAY ; ELIMINATION ; PARKIN ; SIGNAL ; MICE ; DRP1 |
原始文献类型 | Article |
引用统计 | 正在获取...
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文献类型 | 期刊论文 |
条目标识符 | https://kms.shanghaitech.edu.cn/handle/2MSLDSTB/30582 |
专题 | 生命科学与技术学院_硕士生 生命科学与技术学院_特聘教授组_尹慧勇组 |
通讯作者 | Bayir, Hulya; Ji, Jing |
作者单位 | 1.Nanjing Med Univ, Affiliated Hosp 1, Dept Neurosurg, Nanjing 210029, Jiangsu, Peoples R China 2.Nanjing Med Univ, Affiliated Hosp 1, Dept Orthoped, Nanjing 210029, Jiangsu, Peoples R China 3.Univ Pittsburgh, Ctr Free Rad & Antioxidant Hlth, Dept Environm & Occupat Hlth, Pittsburgh, PA 15219 USA 4.Univ Pittsburgh, Dept Crit Care Med, Safar Ctr Resuscitat Res, Pittsburgh, PA 15219 USA 5.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Food Safety Res, Shanghai 200031, Peoples R China 6.Univ Chinese Acad Sci, CAS, Beijing 100049, Peoples R China 7.Shanghai Tech Univ, Sch Life Sci & Technol, Shanghai 201210, Peoples R China 8.Nanjing Univ, Sch Med, Dept Med Genet, Nanjing 210093, Jiangsu, Peoples R China 9.Jiangsu Key Lab Mol Med, Nanjing 210029, Jiangsu, Peoples R China 10.Minist Hlth, Key Lab Food Safety Risk Assessment, Beijing 100022, Peoples R China 11.IM Sechenov Moscow State Med Univ, Lab Nav Redox Lipid, Moscow 119991, Russia 12.IM Sechenov Moscow State Med Univ, Dept Human Pathol, Moscow 119991, Russia 13.Childrens Hosp Pittsburgh, Childrens Neurosci Inst, Pittsburgh, PA 15224 USA |
推荐引用方式 GB/T 7714 | Chao, Honglu,Lin, Chao,Zuo, Qiang,et al. Cardiolipin-Dependent Mitophagy Guides Outcome after Traumatic Brain Injury[J]. JOURNAL OF NEUROSCIENCE,2019,39(10):1930-1943. |
APA | Chao, Honglu.,Lin, Chao.,Zuo, Qiang.,Liu, Yinlong.,Xiao, Mengqing.,...&Ji, Jing.(2019).Cardiolipin-Dependent Mitophagy Guides Outcome after Traumatic Brain Injury.JOURNAL OF NEUROSCIENCE,39(10),1930-1943. |
MLA | Chao, Honglu,et al."Cardiolipin-Dependent Mitophagy Guides Outcome after Traumatic Brain Injury".JOURNAL OF NEUROSCIENCE 39.10(2019):1930-1943. |
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