miR-133a enhances the protective capacity of cardiac progenitors cells after myocardial infarction

Stem Cell Reports. 2014 Dec 9;3(6):1029-42. doi: 10.1016/j.stemcr.2014.10.010. Epub 2014 Nov 20.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cardiomegaly / genetics
  • Cardiomegaly / pathology
  • Computational Biology
  • Gene Expression
  • Gene Expression Profiling
  • MicroRNAs / genetics*
  • Myoblasts, Cardiac / metabolism*
  • Myocardial Infarction / genetics*
  • Myocardial Infarction / pathology
  • Myocardial Infarction / physiopathology
  • RNA Interference
  • RNA, Messenger / genetics
  • Rats


  • MIRN1 microRNA, rat
  • MIRN133 microRNA, rat
  • MicroRNAs
  • RNA, Messenger