Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Nat Commun. 2014 Jun 5;5:4063. doi: 10.1038/ncomms5063.

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

Author information

  • 1Division of Genetics, Boston Children's Hospital, Boston, Massachusetts 02115, USA.
  • 21] Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Boston, Massachusetts 02115, USA [2].
  • 31] Division of Genetics, Boston Children's Hospital, Boston, Massachusetts 02115, USA [2].
  • 4Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Boston, Massachusetts 02115, USA.

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-cadherin(Cre) 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.

PMID:
24898859
[PubMed - in process]
PMCID:
PMC4084855
[Available on 2014/12/5]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group
    Loading ...
    Write to the Help Desk