Stem Cell Reports
Volume 3, Issue 6, 9 December 2014, Pages 1029-1042
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Article
miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction

https://doi.org/10.1016/j.stemcr.2014.10.010Get rights and content
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Highlights

  • miR-1 and miR-133a have a role in adult cardiac progenitor cells (CPCs)

  • miR-133a-CPCs protect cardiac function

  • miR-133a-CPCs increase vascularization and protect against hypertrophy

  • miR-133a is enriched in CPCs-derived exosomes

Summary

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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This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).

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Co-first author