Department of Anesthesiology, Affiliated Hospital of Qingdao University Medical College, Qingdao, 266003, Shandong, China.
J Neural Transm (Vienna). 2014 Jun;121(6):593-600. doi: 10.1007/s00702-014-1166-6. Epub 2014 Feb 8.
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.
线粒体钙单向转运体（MCU）将 Ca2+从细胞质转运到线粒体基质，从而维持 Ca2+的内稳态。先前的研究报告称，MCU 被钌红（RR）抑制可保护大脑免受缺血/再灌注（I/R）损伤，线粒体分裂在 I/R 损伤中发挥重要作用。然而，目前尚不清楚 MCU 是否会影响线粒体分裂。本研究发现，RR 处理可降低线粒体中游离钙的浓度、钙调磷酸酶酶活性和动力相关蛋白 1 的表达，而在大脑中动脉阻塞 2 小时后再灌注 24 小时的生物体内， spermine 的处理则产生相反的效果。这些结果表明，MCU 可能通过调节线粒体 Ca2+摄取与线粒体分裂有关，MCU 与线粒体分裂之间的这种关系可能会保护大脑免受 I/R 损伤。
