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Basal lamina remodeling at the skeletal muscle stem cell niche mediates stem cell self-renewal

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Listed:
  • Shantisree Sandeepani Rayagiri

    (University of Sheffield, Firth Court
    South Mimms)

  • Daniele Ranaldi

    (University of Sheffield, Firth Court)

  • Alexander Raven

    (University of Sheffield, Firth Court
    University of Edinburgh)

  • Nur Izzah Farhana Mohamad Azhar

    (University of Sheffield, Firth Court
    Oxford Publishing (Malaysia))

  • Olivier Lefebvre

    (Inserm U1109 MN3T
    Université de Strasbourg
    LabEx Medalis Université de Strasbourg
    Fédération de Médecine Translationnelle de Strasbourg (FMTS))

  • Peter S Zammit

    (New Hunt’s House)

  • Anne-Gaëlle Borycki

    (University of Sheffield, Firth Court)

Abstract

A central question in stem cell biology is the relationship between stem cells and their niche. Although previous reports have uncovered how signaling molecules released by niche cells support stem cell function, the role of the extra-cellular matrix (ECM) within the niche is unclear. Here, we show that upon activation, skeletal muscle stem cells (satellite cells) induce local remodeling of the ECM and the deposition of laminin-α1 and laminin-α5 into the basal lamina of the satellite cell niche. Genetic ablation of laminin-α1, disruption of integrin-α6 signaling or blocking matrix metalloproteinase activity impairs satellite cell expansion and self-renewal. Collectively, our findings establish that remodeling of the ECM is an integral process of stem cell activity to support propagation and self-renewal, and may explain the effect laminin-α1-containing supports have on embryonic and adult stem cells, as well as the regenerative activity of exogenous laminin-111 therapy.

Suggested Citation

  • Shantisree Sandeepani Rayagiri & Daniele Ranaldi & Alexander Raven & Nur Izzah Farhana Mohamad Azhar & Olivier Lefebvre & Peter S Zammit & Anne-Gaëlle Borycki, 2018. "Basal lamina remodeling at the skeletal muscle stem cell niche mediates stem cell self-renewal," Nature Communications, Nature, vol. 9(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03425-3
    DOI: 10.1038/s41467-018-03425-3
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