Izarra, AlbertoMoscoso, IsabelLevent, ElifCanon, SusanaCerrada, InmaculadaDiez-Juan, AntonioBlanca, VanessaNunez-Gil, Ivan-J.Valiente, IñigoRuiz-Sauri, AmparoSepulveda, PilarTiburcy, MalteZimmermann, Wolfram-H.Bernad, Antonio2017-12-012017-12-012014Stem Cell Reports. 2014; 3(6):1029-422213-6711http://hdl.handle.net/20.500.12105/5533miR-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.engVoRhttp://creativecommons.org/licenses/by-nc-nd/4.0/ENGINEERED HEART-TISSUEEMBRYONIC STEM-CELLSOXIDATIVE STRESSMUSCLEDIFFERENTIATIONMICRORNAHYPERTROPHYAPOPTOSISGROWTHREGENERATIONAttribution-NonCommercial-NoDerivatives 4.0 Internacional2546586931029-104210.1016/j.stemcr.2014.10.010Stem Cell Reportsopen access