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

• Published in: Biochemical and biophysical research communications 2009-04, Vol.381 (4), p.597-601
• Main Authors: 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
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Disease Models, Animal; Gene expression; Hypoxia; IGF-1; Insulin-Like Growth Factor I - genetics; Insulin-Like Growth Factor I - metabolism; Ischemia; MicroRNAs; MicroRNAs - biosynthesis; Myocardial infarction; Myocardial Infarction - genetics; Myocardial Infarction - metabolism; Myocardial Infarction - pathology; Rats; Rats, Sprague-Dawley; Serum deprivation; Transcription, Genetic; Up-Regulation
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2009.02.097

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