Role of satellite cells versus myofibers in muscle hypertrophy induced by inhibition of the myostatin/activin signaling pathway

Se Jin Lee, Thanh V. Huynh, Yun Sil Lee, Suzanne M. Sebald, Sarah A. Wilcox-Adelman, Naoki Iwamori, Christoph Lepper, Martin M. Matzuk, Chen Ming Fan

研究成果: ジャーナルへの寄稿学術誌査読

123 被引用数 (Scopus)

抄録

Myostatin and activin A are structurally related secreted proteins that act to limit skeletal muscle growth. The cellular targets for myostatin and activin A in muscle and the role of satellite cells in mediating muscle hypertrophy induced by inhibition of this signaling pathway have not been fully elucidated. Here we show that myostatin/activin A inhibition can cause muscle hypertrophy in mice lacking either syndecan4 or Pax7, both of which are important for satellite cell function and development. Moreover, we show that muscle hypertrophy after pharmacological blockade of this pathway occurs without significant satellite cell proliferation and fusion to myofibers and without an increase in the number of myonuclei per myofiber. Finally, we show that genetic ablation of Acvr2b, which encodes a high-affinity receptor for myostatin and activin A specifically in myofibers is sufficient to induce muscle hypertrophy. All of these findings are consistent with satellite cells playing little or no role in myostatin/activin A signaling in vivo and render support that inhibition of this signaling pathway can be an effective therapeutic approach for increasing muscle growth even in disease settings characterized by satellite cell dysfunction.

本文言語英語
ページ(範囲)E2353-E2360
ジャーナルProceedings of the National Academy of Sciences of the United States of America
109
35
DOI
出版ステータス出版済み - 8月 28 2012
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 一般

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