ArticleThe American journal of pathology2011
Slow-adhering stem cells derived from injured skeletal muscle have improved regenerative capacity.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Mouse Models of Muscle Fibrosis: Mechanisms, Methods, and Applications.Biomedicines · 2026Review
- Dedifferentiation andMolecular medicine reports · 2022Review
- Hypoxia in Cell Reprogramming and the Epigenetic Regulations.Frontiers in cell and developmental biology · 2021Review
- Functional Neuronal Differentiation of Injury-Induced Muscle-Derived Stem Cell-Like Cells with Therapeutic Implications.Scientific reports · 2017Article
- Characterization of an Injury Induced Population of Muscle-Derived Stem Cell-Like Cells.Scientific reports · 2015Article
- Article
- Cellular players in skeletal muscle regeneration.BioMed research international · 2014Review
- Recent advances in Duchenne muscular dystrophy.Degenerative neurological and neuromuscular disease · 2012Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A wide variety of myogenic cell sources have been used for repair of injured and diseased muscle including muscle stem cells, which can be isolated from skeletal muscle as a group of slow-adhering cells on a collagen-coated surface. The therapeutic use of muscle stem cells for improving muscle regeneration is promising; however, the effect of injury on their characteristics and engraftment potential has yet to be described. In the present study, slow-adhering stem cells (SASCs) from both laceration-injured and control noninjured skeletal muscles in mice were isolated and studied. Migration and proliferation rates, multidifferentiation potentials, and differences in gene expression in both groups of cells were compared in vitro. Results demonstrated that a larger population of SASCs could be isolated from injured muscle than from control noninjured muscle. In addition, SASCs derived from injured muscle demonstrated improved migration, a higher rate of proliferation and multidifferentiation, and increased expression of Notch1, STAT3, Msx1, and MMP2. Moreover, when transplanted into dystrophic muscle in MDX/SCID mice, SASCs from injured muscle generated greater engraftments with a higher capillary density than did SASCs from control noninjured muscle. These data suggest that traumatic injury may modify stem cell characteristics through trophic factors and improve the transplantation potential of SASCs in alleviating skeletal muscle injuries and diseases.
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