Literature DB >> 21357194

Cardiac mesenchymal stem cells contribute to scar formation after myocardial infarction.

Signe Carlson1, JoAnn Trial, Christian Soeller, Mark L Entman.   

Abstract

AIMS: Therapeutic advances in prevention and treatment of myocardial infarction (MI) have decreased patient mortality and increased concern about efficient repair and scar formation, processes that are necessary to attenuate complications such as adverse remodelling and heart failure. Since the rapid accumulation and activity of cardiac fibroblasts is critical for proper scar formation, we hypothesized that infarct fibroblasts are generated by a cardiac-resident progenitor cell population. METHODS AND
RESULTS: We found that infarct fibroblasts in C57BL/6 mice are generated by a mesenchymal stem cell (MSC) population that responds robustly to injury by proliferating and accumulating in the infarct. We report that stem cell-derived fibroblasts contribute to the formation of a scar after an infarction by differentiating into matrix-producing fibroblasts closely associated with fibrillar collagen in the infarct. Further characterization of these cells revealed a heterogenous population with expression of both stem cell and canonical cardiac fibroblast markers, suggesting that some have a commitment to the fibroblast phenotype. Our in vitro study of these cells shows that they have extended self-renewal capability and express the primitive marker Nanog. In keeping with these observations, we also report that these cells are multipotent and differentiate readily into fibroblasts as well as other mesenchymal lineages.
CONCLUSION: Cells with the properties of MSCs participate in wound healing after MI in the adult heart.

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Year:  2011        PMID: 21357194      PMCID: PMC3112022          DOI: 10.1093/cvr/cvr061

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  34 in total

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2.  Differential effects of progenitor cell populations on left ventricular remodeling and myocardial neovascularization after myocardial infarction.

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5.  Interleukin-10 Inhibits Bone Marrow Fibroblast Progenitor Cell-Mediated Cardiac Fibrosis in Pressure-Overloaded Myocardium.

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Review 7.  Targeting cardiac fibroblasts to treat fibrosis of the heart: focus on HDACs.

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Review 8.  Stem cell mechanisms during left ventricular remodeling post-myocardial infarction: Repair and regeneration.

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9.  Knockdown of Plakophilin 2 Downregulates miR-184 Through CpG Hypermethylation and Suppression of the E2F1 Pathway and Leads to Enhanced Adipogenesis In Vitro.

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10.  Role of adenosine A2B receptor signaling in contribution of cardiac mesenchymal stem-like cells to myocardial scar formation.

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Journal:  Purinergic Signal       Date:  2014-03-01       Impact factor: 3.765

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