Satellite cells (SATC), the most abundant skeletal muscle stem cells, play a main role in muscle plasticity, including the adaptive response following physical activity. Thus, we investigated how long-term phenotype selection of male mice for high running performance (Dummerstorf high Treadmill Performance; DUhTP) affects abundance, creatine kinase activity, myogenic marker expression (Pax7, MyoD), and functionality (growth kinetics, differentiation) of SATC and their progeny. SATC were isolated from sedentary male DUhTP and control (Dummerstorf Control; DUC) mice at days 12, 43, and 73 of life and after voluntary wheel running for three weeks (day 73). Marked line differences occur at days 43 and 73 (after activity). At both ages, analysis of SATC growth via xCELLigence system revealed faster activation accompanied by a higher proliferation rate and lower proportion of Pax7+ cells in DUhTP mice, indicating reduced reserve cell formation and faster transition into differentiation. Cultures from sedentary DUhTP mice contain an elevated proportion of actively proliferating Pax7+/MyoD+ cells and have a higher fusion index leading to the formation of more large and very large myotubes at day 43. This robust hypertrophic response occurs without any functional load in the donor mice. Thus, our selection model seems to recruit myogenic precursor cells/SATC with a lower activation threshold that respond more rapidly to external stimuli and are more primed for differentiation at the expense of more primitive cells.
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http://dx.doi.org/10.3390/cells11061001 | DOI Listing |
Int J Biol Macromol
January 2025
Sanya Research Institute of Nanjing Agricultural University, Nanjing Agricultural University, Sanya 572025, China; Jiangsu Livestock Embryo Engineering Laboratory, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China. Electronic address:
The post-transcriptional regulation of epigenetic modification is a hot topic in skeletal muscle development research. Both m6A modifications and miRNAs have been well-established as crucial regulators in skeletal muscle development. However, the interacting regulatory mechanisms between m6A modifications and miRNAs in skeletal muscle development remain unclear.
View Article and Find Full Text PDFNPJ Regen Med
December 2024
Orthopedic Research Laboratories, Leni & Peter W. May Department of Orthopedics, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Skeletal muscle regeneration and functional recovery after minor injuries requires the activation of muscle-resident myogenic muscle stem cells (i.e. satellite cells) and their subsequent differentiation into myoblasts, myocytes, and ultimately myofibers.
View Article and Find Full Text PDFMech Ageing Dev
February 2025
Department of Anatomy and Molecular Embryology, Institute of Anatomy, Medical Faculty, Ruhr University Bochum, Bochum, Germany. Electronic address:
Developmental defects of the ventral abdominal wall, such as gastroschisis, have been associated with prenatal stress exposure. To investigate this further, dexamethasone (DEX), a synthetic glucocorticoid, was administered to fertilized chicken eggs on day 1 of incubation to simulate stress, and embryonic development was subsequently analyzed through in-situ hybridization, immunohistochemistry, and histological methods. Significant developmental abnormalities were displayed by DEX-treated embryos, including open abdomens, reduced MYOG expression in the abdominal wall, and disrupted muscle fiber formation, as indicated by altered Myosin heavy chain patterns.
View Article and Find Full Text PDFCell Mol Life Sci
November 2024
Sanya Institute of Nanjing Agricultural University, Nanjing Agricultural University, Nanjing, 210095, China.
Ythdf2 is known to mediate mRNA degradation in an mA-dependent manner, and it has been shown to play a role in skeletal muscle differentiation. Recently, Ythdf2 was also found to bind to mA-modified precursor miRNAs and regulate their maturation. However, it remains unknown whether this mechanism is related to the regulation of myogenesis by Ythdf2.
View Article and Find Full Text PDFMol Cancer Res
November 2024
National Cancer Institute, Frederick, MD, United States.
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