下调和上调
线粒体
细胞生物学
氧化应激
化学
小RNA
细胞凋亡
程序性细胞死亡
癌症研究
生物
生物化学
基因
作者
Yan Huang,Songyun Deng,Yuhang Ai,Yunan Mo,Wenchao Li,Qianyi Peng,Huang Li,Lina Zhang
标识
DOI:10.1007/s11011-020-00666-4
摘要
Micro-RNA125b (miR-125b) and tumor protein p53 (p53) are involved in the regulation of mitochondrial dynamics; however, the mechanism of their possible interaction during oxidative stress remains unclear. In this study, we investigated the role and mechanism of miR-125b and p53 in oxidative stress-induced mitochondrial damage in immortalized mouse hippocampal HT22 cells. Following stimulation with H2O2, we observed downregulation of miR-125b expression, upregulation of p53 expression, mitochondria were damaged and increased cell death. Overexpression of miR-125b alleviated mitochondrial damage and inhibited p53 expression. Furthermore, confocal and electron microscopy showed that overexpression of p53 eliminated the protective effect of miR-125b on the mitochondria. Thus, miR-125b alleviates abnormal mitochondrial homeostasis in H2O2-treated HT22 cells by suppressing p53 expression. Our data reveal a new model by which miR-125b influences mitochondrial dynamics.
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