Expression of MICU1 after experimental focal cerebral ischemia in adult rats
Expression of MICU1 after experimental focal cerebral ischemia in adult rats
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成年大鼠实验性局灶性脑缺血后MICU1的表达
DOI：
10.1186/s41016-017-0078-3
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发表时间：
2017-06
影响因子：
--
通讯作者：
Xiaoyun Liu
中科院分区：
文献类型：
--
作者：
Kun Zhang;Jiajia Yan;Liang Wang;Xinying Tian;Tong Zhang;Bin Li;Wang Wang;Li Guo;Xiaoyun Liu
BackgroundMitochondrial Ca2+uptake is a pivotal pathophysiological process for neuronal survival when subjected to ischemic insult. Mitochondrial calcium uptake 1 (MICU1) has been demonstrated as a key regulator of the mitochondrial calcium uniporter (MCU), identified as a tetrameric highly specific channel that modulates mitochondrial Ca2+uptake.MethodsAdult male Sprague–Dawley (SD) rats underwent middle cerebral artery occlusion (MCAO) to create the standard focal cerebral ischemia model. The permanent MCAO approach utilized the intraluminal approach. Neurological examination, and subsequent histological characterization of cerebral infarcts using triphenyltetrazolium chloride staining, as well as Western blot, immunohistochemical staining, and real-time quantitative polymerase chain reaction assays were employed to assess the functional effects of MICU1 and its expression in the brain.ResultsAnimals exposed to MCAO displayed the typical neurological deficit accompanied by cortical and subcortical infarction at 72 h post-stroke. The expression of MICU1, with co-localization with neurons, was detected at different time points (6 h and 12 h) after ischemic damage. Altogether, these observations revealed an up-regulation of MICU1 expression in the early stages of cerebral ischemia.ConclusionThe results demonstrated that MICU1 was upregulated in neurons at the acute phase of ischemic stroke. Because MICU1 has been previously shown to participate in mitochondrial Ca2+uptake mediated by MCU, our study further implicates the involvement of MICU1 in calcium overload-induced cell death which is closely associated with stroke.
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