MicroRNA-24 regulates cardiac fibrosis after myocardial infarction.
Bottom Line: TGF-β (a pathological mediator of fibrotic disease) increased miR-24 expression, overexpression of miR-24 reduced TGF-β secretion and Smad2/3 phosphorylation in CFs.Finally, we demonstrated that protein and mRNA levels of furin were regulated by miR-24 in CFs.These findings suggest that miR-24 has a critical role in CF function and cardiac fibrosis after MI through a furin-TGF-β pathway.
Affiliation: State Key Laboratory of Translational Cardiovascular Medicine, Fuwai Hospital & Cardiovascular Institute, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.Show MeSH
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Mentions: We previously monitored miRNA expression and cardiac fibrosis in remodelling and reverse remodelling of the heart, and found that changes in the expression of miR-24 were associated with fibrosis. To ascertain if miR-24 is dysregulated during MI, we measured expression of the miR-24 at various time-points and different sections in a mouse model of MI. Expression of the miR-24 transcript was down-regulated after MI; expression peaked 1 week after MI, then gradually attenuated in infarct and remote areas over time, and was finally restored to normal levels at 28 days after MI (Fig. 1A). In the same way, expression of collagen-1, fibronectin and TGF-β1 in different areas in the MI model was detected at different times (Fig. 1B–D), a significant correlation was found between expression of miR-24 and fibrosis level.
Affiliation: State Key Laboratory of Translational Cardiovascular Medicine, Fuwai Hospital & Cardiovascular Institute, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.