miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction
2014 | journal article; research paper. A publication with affiliation to the University of Göttingen.
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miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction
Izarra, A.; Moscoso, I.; Levent, E. ; Canon, S.; Cerrada, I.; Diez-Juan, A. & Blanca, V. et al. (2014)
Stem Cell Reports, 3(6) pp. 1029-1042. DOI: https://doi.org/10.1016/j.stemcr.2014.10.010
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- Authors
- Izarra, Alberto; Moscoso, Isabel; Levent, Elif ; Canon, Susana; Cerrada, Inmaculada; Diez-Juan, Antonio; Blanca, Vanessa; Nunez-Gil, Ivan-J.; Valiente, Inigo; Ruiz-Sauri, Amparo; Sepulveda, Pilar; Tiburcy, Malte ; Zimmermann, Wolfram-Hubertus ; Bernad, Antonio
- Abstract
- 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.
- Issue Date
- 2014
- Journal
- Stem Cell Reports
- Project
- SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz
SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien
SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle - Working Group
- RG Tiburcy (Stem Cell Disease Modeling)
RG Zimmermann (Engineered Human Myocardium) - ISSN
- 2213-6711