Journal
STEM CELL REPORTS
Volume 3, Issue 6, Pages 1029-1042Publisher
CELL PRESS
DOI: 10.1016/j.stemcr.2014.10.010
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Funding
- Ministry of Economy and Competition [SAF2012-3432, PLE2009-0147, PSE-010000-2009-3]
- Comunidad Autonoma de Madrid [S2011/BMD-2420]
- ISCIII [RD12/0019/0018]
- DZHK (German Center for Cardiovascular Research)
- German Federal Ministry for Science and Education [BMBF FKZ 13GW0007A]
- German Research Foundation [DFG ZI 708/7-1, 8-1, 10-1, SFB 1002 TP C04, TP S]
- NIH [U01 HL099997]
- European Commission [FP7-HEALTH-2009/CARE-MI]
- Ministry of Economy and Competition
- ISCIII
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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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