miR-133a enhances the protective capacity of cardiac progenitors cells after myocardial infarction
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Identificadores
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Fecha de publicación
2014Título de revista
Stem Cell Reports
Tipo de contenido
Artigo
MeSH
Animals | Cardiomegaly | Computational Biology | Gene Expression | Gene Expression Profiling | MicroRNAs | Myoblasts, Cardiac | Myocardial Infarction | RNA Interference | RNA, Messenger | RatsResumen
miR-133a and miR-1 are known as muscle-specific microRNAs that are involved in cardiac development and pathophysiology. We have shown that both miR-1 and miR-133a are early and progressively upregulated during in vitro cardiac differentiation of adult cardiac progenitor cells (CPCs), but only miR-133a expression was enhanced under in vitro oxidative stress. miR-1 was demonstrated to favor differentiation of CPCs, whereas miR-133a overexpression protected CPCs against cell death, targeting, among others, the proapoptotic genes Bim and Bmf. miR-133a-CPCs clearly improved cardiac function in a rat myocardial infarction model by reducing fibrosis and hypertrophy and increasing vascularization and cardiomyocyte proliferation. The beneficial effects of miR-133a-CPCs seem to correlate with the upregulated expression of several relevant paracrine factors and the plausible cooperative secretion of miR-133a via exosomal transport. Finally, an in vitro heart muscle model confirmed the antiapoptotic effects of miR-133a-CPCs, favoring the structuration and contractile functionality of the artificial tissue.
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