Document Detail


miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction.
MedLine Citation:
PMID:  25465869     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
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.
Authors:
Alberto Izarra; Isabel Moscoso; Elif Levent; Susana Cañón; Inmaculada Cerrada; Antonio Díez-Juan; Vanessa Blanca; Iván-J Núñez-Gil; Iñigo Valiente; Amparo Ruíz-Sauri; Pilar Sepúlveda; Malte Tiburcy; Wolfram-H Zimmermann; Antonio Bernad
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-11-20
Journal Detail:
Title:  Stem cell reports     Volume:  -     ISSN:  2213-6711     ISO Abbreviation:  Stem Cell Reports     Publication Date:  2014 Nov 
Date Detail:
Created Date:  2014-12-3     Completed Date:  -     Revised Date:  2014-12-4    
Medline Journal Info:
Nlm Unique ID:  101611300     Medline TA:  Stem Cell Reports     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.
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