2026-06-14T05:05:03Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/55332024-09-27T08:46:21Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Izarra, Alberto author Moscoso, Isabel author Levent, Elif author Canon, Susana author Cerrada, Inmaculada author Diez-Juan, Antonio author Blanca, Vanessa author Nunez-Gil, Ivan-J. author Valiente, Iñigo author Ruiz-Sauri, Amparo author Sepulveda, Pilar author Tiburcy, Malte author Zimmermann, Wolfram-H. author Bernad, Antonio author 2014 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. Stem Cell Reports. 2014; 3(6):1029-42 10.1016/j.stemcr.2014.10.010 2213-6711 Stem Cell Reports 25465869 http://hdl.handle.net/20.500.12105/5533 ENGINEERED HEART-TISSUE EMBRYONIC STEM-CELLS OXIDATIVE STRESS MUSCLE DIFFERENTIATION MICRORNA HYPERTROPHY APOPTOSIS GROWTH REGENERATION miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction