Role of mitochondrial calcium uniporter in regulating mitochondrial fission in the cerebral cortexes of living rats

被引：34

作者：

Liang, Nan ^{[1
]}

Wang, Peng ^{[1
]}

Wang, Shilei ^{[1
]}

Li, Shuhong ^{[1
]}

Li, Yu ^{[1
]}

Wang, Jinying ^{[1
]}

Wang, Min ^{[1
]}

机构：

[1] Qingdao Univ, Coll Med, Affiliated Hosp, Dept Anesthesiol, Qingdao 266003, Shandong, Peoples R China

来源：

JOURNAL OF NEURAL TRANSMISSION | 2014年 / 121卷 / 06期

关键词：

Ischemia/reperfusion injury; MCU; Mitochondrial fission; Mitochondrial calcium; ISCHEMIA/REPERFUSION INJURY; APOPTOSIS; DRP1; DYSFUNCTION; OCCLUSION; DYNAMICS; KINASE; ARTERY;

D O I：

10.1007/s00702-014-1166-6

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

100204 [神经病学];

摘要：

The mitochondrial calcium uniporter (MCU) transports Ca2+ from the cytoplasm to the mitochondrial matrix and thus maintains Ca2+ homeostasis. Previous studies have reported that inhibition of MCU by ruthenium red (RR) protects the brain from ischemia/reperfusion (I/R) injury and that mitochondrial fission plays an important role in I/R injury. However, it is still not known whether MCU affects mitochondrial fission. In the present study, treatment with RR was found to decrease the concentration of free calcium in the mitochondria, calcineurin enzyme activity and dynamin-related protein 1 expression, and treatment with spermine was found to have the opposite effect in organisms subjected to occlusion of the middle cerebral artery lasting 2 h followed by 24 h reperfusion. These results indicate that MCU may be related to mitochondrial fission via modulating mitochondrial Ca2+ uptake and this relationship between MCU and mitochondrial fission may protect the brain from I/R injury.

引用

页码：593 / 600

页数：8

共 29 条

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[2]

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