Mesenchymal progenitors distinct from satellite cells contribute to ectopic fat cell formation in skeletal muscle

Akiyoshi Uezumi, So Ichiro Fukada, Naoki Yamamoto, Shin'Ichi Takeda, Kunihiro Tsuchida

Research output: Contribution to journalArticle

506 Citations (Scopus)

Abstract

Ectopic fat deposition in skeletal muscle is closely associated with several disorders, however, the origin of these adipocytes is not clear, nor is the mechanism of their formation. Satellite cells function as adult muscle stem cells but are proposed to possess multipotency. Here, we prospectively identify PDGFRα+ mesenchymal progenitors as being distinct from satellite cells and located in the muscle interstitium. We show that, of the muscle-derived cell populations, only PDGFRα+ cells show efficient adipogenic differentiation both in vitro and in vivo. Reciprocal transplantations between regenerating and degenerating muscles, and co-culture experiments revealed that adipogenesis of PDGFRα+ cells is strongly inhibited by the presence of satellite cell-derived myofibres. These results suggest that PDGFRα+ mesenchymal progenitors are the major contributor to ectopic fat cell formation in skeletal muscle, and emphasize that interaction between muscle cells and PDGFRα+ mesenchymal progenitors, not the fate decision of satellitecells, has a considerable impact on muscle homeostasis.

Original languageEnglish
Pages (from-to)143-152
Number of pages10
JournalNature Cell Biology
Volume12
Issue number2
DOIs
Publication statusPublished - 01-02-2010

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Adipocytes
Skeletal Muscle
Muscle Cells
Muscles
Adipogenesis
Adult Stem Cells
Coculture Techniques
Homeostasis
Transplantation
Fats
Population

All Science Journal Classification (ASJC) codes

  • Cell Biology

Cite this

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Mesenchymal progenitors distinct from satellite cells contribute to ectopic fat cell formation in skeletal muscle. / Uezumi, Akiyoshi; Fukada, So Ichiro; Yamamoto, Naoki; Takeda, Shin'Ichi; Tsuchida, Kunihiro.

In: Nature Cell Biology, Vol. 12, No. 2, 01.02.2010, p. 143-152.

Research output: Contribution to journalArticle

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