2026-06-14T06:44:05Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/55332024-09-27T08:46:21Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
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
funder
Ministerio de Economía y Competitividad (España)
funder
Comunidad de Madrid (España)
funder
Instituto de Salud Carlos III
funder
German Centre for Cardiovascular Research
funder
Deutsche Forschungsgemeinschaft (Alemania)
funder
National Institutes of Health (Estados Unidos)
funder
Unión Europea. Comisión Europea
2017-12-01T07:37:28Z
2017-12-01T07:37:28Z
2014
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
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.
eng
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
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miR-133aEnhancesTheProtective_2014.pdf
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miR-133aEnhancesTheProtective_2014_SM.pdf
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miR-133aEnhancesTheProtective_2014.pdf.txt
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miR-133aEnhancesTheProtective_2014_SM.pdf.txt