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First published online August 22, 2007
doi: 10.1242/10.1242/jcs.010728
Research Article |
1 Department of Pharmacology (the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), Harbin Medical University, Harbin, Heilongjiang 150086, People's Republic of China
2 Institute of Cardiovascular Research, Harbin Medical University, Harbin, Heilongjiang 150086, People's Republic of China
3 Research Center, Montreal Heart Institute, Montreal, PQ H1T 1C8, Canada
4 Department of Medicine, University of Montreal, Montreal, PQ H3C 3J7, Canada
* Authors for correspondence (e-mails: wz.email{at}gmail.com; yangbf{at}ems.hrbmu.edu.cn)
Accepted 26 June 2007
The microRNAs miR-1 and miR-133 are preferentially expressed in cardiac and skeletal muscles and have been shown to regulate differentiation and proliferation of these cells. We report here a novel aspect of cellular function of miR-1 and miR-133 regulation of cardiomyocyte apoptosis. miR-1 and miR-133 produced opposing effects on apoptosis, induced by oxidative stress in H9c2 rat ventricular cells, with miR-1 being pro-apoptotic and miR-133 being anti-apoptotic. miR-1 level was significantly increased in response to oxidative stress. We identified single target sites for miR-1 only, in the 3'-untranslated regions of the HSP60 and HSP70 genes, and multiple putative target sites for miR-133 throughout the sequence of the caspase-9 gene. miR-1 reduced the levels of HSP60 and HSP70 proteins without changing their transcript levels, whereas miR-133 did not affect HSP60 and HSP70 expression at all. By contrast, miR-133 repressed caspase-9 expression at both the protein and mRNA levels. The post-transcriptional repression of HSP60 and HSP70 and caspase-9 was further confirmed by luciferase reporter experiments. Our results indicate that miR-1 and miR-133 are involved in regulating cell fate with increased miR-1 and/or decreased miR-133 levels favoring apoptosis and decreased miR-1 and/or miR-133 levels favoring survival. Post-transcriptional repression of HSP60 and HSP70 by miR-1 and of caspase-9 by miR-133 contributes significantly to their opposing actions.
Key words: miR-1, miR-133, Apoptosis, HSP60, HSP70, Caspase-9
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