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

被引:219
作者
Shan, Zhi-Xin [1 ]
Lin, Qiu-Xiong [1 ]
Fu, Yong-Heng [1 ]
Deng, Chun-Yu [1 ]
Zhou, Zhi-Ling [1 ]
Zhu, Jie-Ning [1 ]
Liu, Xiao-Ying [1 ]
Zhang, You-Yi [4 ]
Li, Yangxin [2 ,3 ]
Lin, Shu-Guang [1 ]
Yu, Xi-Yong [1 ]
机构
[1] Guangdong Acad Med Sci, Guangdong Prov Cardiovasc Inst, Res Ctr Guangdong Gen Hosp, Guangzhou 510080, Guangdong, Peoples R China
[2] Univ Texas Hlth Sci Ctr, Houston, TX 77030 USA
[3] Texas Heart Inst, Houston, TX 77030 USA
[4] Peking Univ, Inst Vasc Med, Hosp 3, Beijing 100083, Peoples R China
基金
中国国家自然科学基金;
关键词
MicroRNAs; Ischemia; Myocardial infarction; Gene expression; IGF-1; Apoptosis; Serum deprivation; Hypoxia; MUSCLE-SPECIFIC MICRORNA; APOPTOSIS; CONNEXIN-43; DIFFERENTIATION; CARDIOMYOCYTES; MIR-1;
D O I
10.1016/j.bbrc.2009.02.097
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:597 / 601
页数:5
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