Journal
FEBS LETTERS
Volume 589, Issue 22, Pages 3449-3453Publisher
WILEY
DOI: 10.1016/j.febslet.2015.10.004
Keywords
Laminin; Muscle regeneration; Laminin therapy; Muscular disease; Myoblasts transplantation
Funding
- CNPq
- CAPES
- FAPERJ
- Fiocruz (Brazil)
- Focem (Mercosur)
- Faperj-Sorbonne Universites (Brazil-France)
- Association Francaise contre les Myopathies (AFM)
- DPP-Nl
- EU (FP7 Myoage project) [HEALTH-F2-2009-223576]
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Muscle regeneration is essentially due to activation of satellite cells, which can be isolated and amplified ex vivo, thus representing good candidates for cell therapy. Accumulating data show that the local microenvironment plays a major role during muscle regeneration. In the satellite cell niche, a major extracellular matrix protein is laminin. Human myoblasts transplanted into immunodeficient mice are preferentially located in laminin-enriched areas. Additionally, laminin-111 enhances myoblast proliferation in vitro and increases expression of the alpha 7 beta 1 integrin-type laminin receptor. Intramuscular injection of laminin-111 ameliorates muscular pathology in mdx mice, protecting muscle fibers from damage. Moreover, transplantation of human myoblasts with laminin-111 into Rag/mdx immunodeficient recipients improved efficacy of myoblast transplantation, increasing the number of human dystrophin-positive myofibres. Taken together, these data strongly indicate that exogenous laminin can ameliorate the regeneration process in different models of muscular dystrophies and can be instrumental for improving cell therapy aiming at repairing the degeneration/regeneration process in skeletal muscle. (C) 2015 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.
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