AI Article Synopsis
- The study found that as muscles age, there is an increase in nonimmune cells (CD45neg) that have high levels of a stem-cell marker (Sca-1) but are less likely to express a key muscle development protein (MyoD).
- In younger muscles, a much higher percentage of these cells express MyoD, indicating a more regenerative capacity compared to aged muscles.
- The research suggests that these non-myogenic Sca-1 positive cells not only proliferate but also promote fibrosis instead of muscle repair, possibly leading to a decline in muscle regeneration with age.
Article Abstract
We report an age-dependent increase in nonimmunohematopoietic cells (CD45neg) in regenerating muscle characterized by high stem-cell antigen (Sca-1) expression. In aged regenerating muscle, only 14% of these CD45negSca-1pos cells express MyoD, whereas 82% of CD45negSca-1(pos) cells are MyoDpos in young adult muscle. In vitro, CD45negMyoDnegSca-1pos cells overexpress fibrosis-promoting genes, potentially controlled by Wnt2. The cells are proliferative, nonmyogenic, and nonadipogenic, and arise in clonally derived myoblast cultures from aged mice. MyoDneg Sca-1pos nonmyogenic cells also emerge in C2C12 myoblast cultures at late passage. Both in vitro and in vivo studies suggest that MyoDnegSca-1pos cells from aged muscle are more susceptible to apoptosis than myoblasts, which may contribute to depletion of the satellite cell pool. Thus, with age, a subset of myoblasts takes on an altered phenotype, which is marked by high Sca-1 expression. These cells do not participate in muscle regeneration, and instead may contribute to muscle fibrosis in aged muscle.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755567 | PMC |
| http://dx.doi.org/10.1093/gerona/63.6.566 | DOI Listing |
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