MiR-210在缺氧中调控机制的研究进展  

The Research Progress of MiR-210 and its Regulation Mechanisms in Hypoxia

作　　者：史孟婧[1] 赵远鹏[1] 邹仲敏[1] 赛燕[1] 赵吉清[1] 

机构地区：[1]第三军医大学军事预防医学院毒理学研究所,重庆400038

出　　处：《现代生物医学进展》2013年第16期3173-3175,共3页Progress in Modern Biomedicine

基　　金：全军医学科技十二五科研项目重点项目(BWS11R02)

摘　　要：MicroRNA(miRNA)是一类包含21-25个核苷酸的单链非编码小RNA。研究表明,miR-210可直接抑制线粒体内铁硫蛋白(Fe-S)的支架蛋白ISCU1/2的表达从而抑制线粒体代谢;miR-210对DNA损伤修复基因-RAD家族有抑制作用,减弱了DNA修复能力;miR-210可以通过调节E2F3、纤维母细胞生长因子受体1(FGFRL1)、同源域基因A1(HOXA1)等阻止细胞增殖,调控细胞周期;缺氧刺激可上调miR-210表达,这对促进血管再生有重要作用。miR-210的表达受缺氧诱导,调控缺氧反应相关基因的表达,提示miR-210有可能成为诊治包括缺血性损伤、肿瘤在内等多种疾病的新靶点。MicroRNAs（miRNA） are 21-25-nucleotide,single-stranded,non-coding RNAs.Recent studies have shown that miR-210 directly repress the mitochondrial metabolism by suppressing the expression of ISCU1/2,which is a scaffolding protein of Fe-S protein.What＇ more,miR-210 is able to arrest DNA repair by repressing the DNA repaire gene-RAD.By regulating E2F3,FGFR1 and HOXA1 etc,miR-210 restrains cell proliferation and cell cycle.The expression of miR-210 is elevated by hypoxia,which plays an important role in promoting angiogenesis.The expression of miR-210 is hypoxia inducible,and subsequently regulates the expression of genes relative to hypoxia response.Present data suggest that miR-210 may become a novel sensitive biomarker and therapeutic target for the clinical diagnosis and prognosis of many diseases including ischemic injury and tumour.

关 键 词：MIR-210 缺氧 DNA修复 线粒体 血管再生 

分 类 号：Q75[生物学—分子生物学] Q78