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Intramuscular adipogenesis is inhibited by myo-endothelial progenitors with functioning Bmpr1a signalling

Author

Listed:
  • Ping Huang

    (Boston Children’s Hospital)

  • Tim J. Schulz

    (Section on Integrative Physiology and Metabolism, Joslin Diabetes Center
    Present address: Department of Adipocyte Development, German Institute of Human Nutrition Potsdam-Rehbrücke, 14558 Nuthetal, Germany)

  • Ariane Beauvais

    (Boston Children’s Hospital
    Present address: Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada K1Y 4E9)

  • Yu-Hua Tseng

    (Section on Integrative Physiology and Metabolism, Joslin Diabetes Center)

  • Emanuela Gussoni

    (Boston Children’s Hospital)

Abstract

Developing human muscle contains inter-myofibre progenitors expressing Bmp-receptor 1a (Bmpr1a) and Myf5 that respond to stimulation with Bmp4. Here we ablate Bmpr1a in Myf5- and MyoD-expressing cells in vivo. Mutant mice reveal increased intramuscular fat and reduced myofibre size in selected muscles, or following muscle injury. Myo-endothelial progenitors are the most affected cell type: clonal studies demonstrate that ablation of Bmpr1a in myo-endothelial cells results in decreased myogenic activity, while adipogenic differentiation is significantly increased. Downstream phospho-Smad 1, 5, 8 signalling is also severely decreased in mutant myo-endothelial cells. Lineage tracing of endothelial cells using VE-cadherinCre driver failed to reveal a significant contribution of these cells to developing or injured skeletal muscle. Thus, myo-endothelial progenitors with functioning Bmpr1a signalling demonstrate myogenic potential, but their main function in vivo is to inhibit intramuscular adipogenesis, both through a cell-autonomous and a cell–cell interaction mechanism.

Suggested Citation

  • Ping Huang & Tim J. Schulz & Ariane Beauvais & Yu-Hua Tseng & Emanuela Gussoni, 2014. "Intramuscular adipogenesis is inhibited by myo-endothelial progenitors with functioning Bmpr1a signalling," Nature Communications, Nature, vol. 5(1), pages 1-16, September.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5063
    DOI: 10.1038/ncomms5063
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