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miR-195/497 induce postnatal quiescence of skeletal muscle stem cells

Author

Listed:
  • Takahiko Sato

    (Institute for Frontier Medical Sciences, Kyoto University)

  • Takuya Yamamoto

    (Center for iPS Cell Research and Application, Kyoto University
    Institute for Integrated Cell-Material Sciences (WPI-iCeMS), Kyoto University)

  • Atsuko Sehara-Fujisawa

    (Institute for Frontier Medical Sciences, Kyoto University)

Abstract

Skeletal muscle stem cells (MuSCs), the major source for skeletal muscle regeneration in vertebrates, are in a state of cell cycle arrest in adult skeletal muscles. Prior evidence suggests that embryonic muscle progenitors proliferate and differentiate to form myofibres and also self-renew, implying that MuSCs, derived from these cells, acquire quiescence later during development. Depletion of Dicer in adult MuSCs promoted their exit from quiescence, suggesting microRNAs are involved in the maintenance of quiescence. Here we identified miR-195 and miR-497 that induce cell cycle arrest by targeting cell cycle genes, Cdc25 and Ccnd. Reduced expression of MyoD in juvenile MuSCs, as a result of overexpressed miR-195/497 or attenuated Cdc25/Ccnd, revealed an intimate link between quiescence and suppression of myogenesis in MuSCs. Transplantation of cultured MuSCs treated with miR-195/497 contributed more efficiently to regenerating muscles of dystrophin-deficient mice, indicating the potential utility of miR-195/497 for stem cell therapies.

Suggested Citation

  • Takahiko Sato & Takuya Yamamoto & Atsuko Sehara-Fujisawa, 2014. "miR-195/497 induce postnatal quiescence of skeletal muscle stem cells," Nature Communications, Nature, vol. 5(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5597
    DOI: 10.1038/ncomms5597
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    1. Gareth Hawkes & Robin N. Beaumont & Zilin Li & Ravi Mandla & Xihao Li & Christine M. Albert & Donna K. Arnett & Allison E. Ashley-Koch & Aneel A. Ashrani & Kathleen C. Barnes & Eric Boerwinkle & Jenni, 2024. "Whole-genome sequencing in 333,100 individuals reveals rare non-coding single variant and aggregate associations with height," Nature Communications, Nature, vol. 15(1), pages 1-11, December.

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