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心肌梗死大鼠模型中miR-1/miR-206的表达上调

Upregulated expression of miR-1/miR-206 in a rat model of myocardial infarction.

作者信息

Shan Zhi-Xin, Lin Qiu-Xiong, Fu Yong-Heng, Deng Chun-Yu, Zhou Zhi-Ling, Zhu Jie-Ning, Liu Xiao-Ying, Zhang You-Yi, Li Yangxin, Lin Shu-Guang, Yu Xi-Yong

机构信息

Research Center of Guangdong General Hospital, Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, China.

出版信息

Biochem Biophys Res Commun. 2009 Apr 17;381(4):597-601. doi: 10.1016/j.bbrc.2009.02.097. Epub 2009 Feb 24.

Abstract

MicroRNAs (miRNAs) have been increasingly reported to have important roles in diverse biological and pathological processes. We investigated miR-1 and miR-206 expression and their potential roles in a rat model of myocardial infarction (MI). miR-1 and miR-206 expression were significantly increased, and insulin-like growth factor 1 (IGF-1) protein was markedly reduced without obvious change of its mRNA level after MI induction. Position 175-196 of rat IGF-1 3'-untranslated region was identified to be required for efficient downregulation by miR-1/miR-206. IGF-1 level was reduced without changing its transcript level in rat H9C2 myoblast cells modified with miR-1 (H9C2-miR-1). In the serum withdrawal and hypoxic condition, caspase-3 activity and mitochondrial potential were significantly increased in H9C2-miR-1 cells compared with the control group, respectively (p<0.05, p<0.01). Together, our results indicate that miR-1 and miR-206 are involved in apoptotic cell death in MI by post-transcriptional repression of IGF-1.

摘要

越来越多的报道表明,微小RNA(miRNA)在多种生物学和病理过程中发挥着重要作用。我们研究了miR-1和miR-206在大鼠心肌梗死(MI)模型中的表达及其潜在作用。MI诱导后,miR-1和miR-206的表达显著增加,胰岛素样生长因子1(IGF-1)蛋白明显减少,但其mRNA水平无明显变化。大鼠IGF-1 3'-非翻译区的175-196位被确定为miR-1/miR-206有效下调所必需的区域。在用miR-1修饰的大鼠H9C2成肌细胞(H9C2-miR-1)中,IGF-1水平降低,但其转录水平未改变。在血清饥饿和缺氧条件下,与对照组相比,H9C2-miR-1细胞中的caspase-3活性和线粒体电位分别显著增加(p<0.05,p<0.01)。总之,我们的结果表明,miR-1和miR-206通过对IGF-1的转录后抑制参与MI中的凋亡细胞死亡。

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