微小RNA-761通过靶向线粒体分裂因子来调控线粒体网络。
miR-761 regulates the mitochondrial network by targeting mitochondrial fission factor.
作者信息
Long Bo, Wang Kun, Li Na, Murtaza Iram, Xiao Jing-Ying, Fan Yuan-Yuan, Liu Cui-Yun, Li Wen-Hui, Cheng Zheng, Li PeiFeng
机构信息
Division of Cardiovascular Research, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.
Division of Cardiovascular Research, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China; Signal Transduction Laboratory, Department of Biochemistry, Quaid-i-Azam University, 45320 Islamabad, Pakistan.
出版信息
Free Radic Biol Med. 2013 Dec;65:371-379. doi: 10.1016/j.freeradbiomed.2013.07.009. Epub 2013 Jul 15.
Mitochondria are dynamic organelles that constantly undergo fission and fusion. The balance between fission and fusion determines the fate of the cell. In this study, we show that mitochondrial fission factor (MFF) is upregulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. Knockdown of MFF attenuated hydrogen peroxide- and I/R injury-induced cardiomyocyte apoptosis and myocardial infarction. We found that MFF is a direct target of miR-761, and miR-761 inhibits mitochondrial fission and cardiomyocyte apoptosis by repressing MFF. This study reveals a novel model of mitochondrial fission regulation, which is composed of miR-761 and MFF. Modulation of their levels may provide a new approach for tackling apoptosis and myocardial infarction.
线粒体是动态细胞器，不断经历分裂和融合。分裂与融合之间的平衡决定细胞的命运。在本研究中，我们表明，过氧化氢处理或缺血/再灌注（I/R）损伤后，线粒体分裂因子（MFF）上调。敲低MFF可减轻过氧化氢和I/R损伤诱导的心肌细胞凋亡和心肌梗死。我们发现MFF是miR-761的直接靶点，miR-761通过抑制MFF来抑制线粒体分裂和心肌细胞凋亡。本研究揭示了一种由miR-761和MFF组成的线粒体分裂调控新模型。调节它们的水平可能为解决细胞凋亡和心肌梗死提供一种新方法。
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