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Laminin regulates PDGFRβ+ cell stemness and muscle development

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Listed:
  • Yao Yao

    (Laboratory of Neurobiology and Genetics, The Rockefeller University
    College of Pharmacy, University of Minnesota)

  • Erin H. Norris

    (Laboratory of Neurobiology and Genetics, The Rockefeller University)

  • Christopher E. Mason

    (Weill Cornell Medical College
    The HRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine
    Tri-Institutional Training Program in Computational Biology and Medicine
    The Feil Family Brain and Mind Research Institute)

  • Sidney Strickland

    (Laboratory of Neurobiology and Genetics, The Rockefeller University)

Abstract

Muscle-resident PDGFRβ+ cells, which include pericytes and PW1+ interstitial cells (PICs), play a dual role in muscular dystrophy. They can either undergo myogenesis to promote muscle regeneration or differentiate into adipocytes and other cells to compromise regeneration. How the differentiation and fate determination of PDGFRβ+ cells are regulated, however, remains unclear. Here, by utilizing a conditional knockout mouse line, we report that PDGFRβ+ cell-derived laminin inhibits their proliferation and adipogenesis, but is indispensable for their myogenesis. In addition, we show that laminin alone is able to partially reverse the muscle dystrophic phenotype in these mice at the molecular, structural and functional levels. Further RNAseq analysis reveals that laminin regulates PDGFRβ+ cell differentiation/fate determination via gpihbp1. These data support a critical role of laminin in the regulation of PDGFRβ+ cell stemness, identify an innovative target for future drug development and may provide an effective treatment for muscular dystrophy.

Suggested Citation

  • Yao Yao & Erin H. Norris & Christopher E. Mason & Sidney Strickland, 2016. "Laminin regulates PDGFRβ+ cell stemness and muscle development," Nature Communications, Nature, vol. 7(1), pages 1-15, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11415
    DOI: 10.1038/ncomms11415
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