Literature DB >> 18805052

Characterization of the paracrine effects of human skeletal myoblasts transplanted in infarcted myocardium.

Maitane Perez-Ilzarbe1, Onnik Agbulut, Beatriz Pelacho, Cristina Ciorba, Edurne San Jose-Eneriz, Michel Desnos, Albert A Hagège, Pablo Aranda, Enrique J Andreu, Philippe Menasché, Felipe Prósper.   

Abstract

BACKGROUND: The discrepancy between the functional improvements yielded experimentally by skeletal myoblasts (SM) transplanted in infarcted myocardium and the paucity of their long-term engraftment has raised the hypothesis of cell-mediated paracrine mechanisms. METHODS AND
RESULTS: We analyzed gene expression and growth factors released by undifferentiated human SM (CD56(+)), myotubes (SM cultured until confluence) and fibroblasts-like cells (CD56(-)). Gene expression revealed up-regulation of pro-angiogenic (PGF), anti-apoptotics (BAG-1, BCL-2), heart development (TNNT2, TNNC1) and extracellular matrix remodelling (MMP-2, MMP-7) genes in SM. In line with the gene expression profile, the analysis of culture supernatants of SM by ELISA identified the release of growth factors involved in angiogenesis (VEGF, PIGF, angiogenin, angiopoietin, HGF and PDGF-BB) as well as proteases involved in matrix remodelling (MMP2, MMP9 and MMP10) and their inhibitors (TIMPs). Culture of smooth muscle cells (SMC), cardiomyocytes (HL-1) and human umbilical vein endothelial cells (HUVECs) with SM-released conditioned media demonstrated an increased proliferation of HUVEC, SMC and cardiomyocytes (p<0.05) and a decrease in apoptosis of cardiomyocytes (p<0.05). Analysis of nude rats transplanted with human SM demonstrated expression of human-specific MMP-2, TNNI3, CNN3, PGF, TNNT2, PAX7, TGF-beta, and IGF-1 1 month after transplant.
CONCLUSIONS: Our data support the paracrine hypothesis whereby myoblast-secreted factors may contribute to the beneficial effects of myogenic cell transplantation in infarcted myocardium.

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Year:  2008        PMID: 18805052     DOI: 10.1016/j.ejheart.2008.08.002

Source DB:  PubMed          Journal:  Eur J Heart Fail        ISSN: 1388-9842            Impact factor:   15.534


  58 in total

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