Possible role of TIEG1 as a feedback regulator of myostatin and TGF-β in myoblasts

Masato Miyake, Shinichiro Hayashi, Shunsuke Iwasaki, Guozheng Chao, Hideyuki Takahashi, Kouichi Watanabe, Shyuichi Ohwada, Hisashi Aso, Takahiro Yamaguchi

研究成果: Contribution to journalArticle査読

13 被引用数 (Scopus)

抄録

Myostatin and TGF-β negatively regulate skeletal muscle development and growth. Both factors signal through the Smad2/3 pathway. However, the regulatory mechanism of myostatin and TGF-β signaling remains unclear. TGF-β inducible early gene (TIEG) 1 is highly expressed in skeletal muscle and has been implicated in the modulation of TGF-β signaling. These findings prompted us to investigate the effect of TIEG1 on myostatin and TGF-β signaling using C2C12 myoblasts. Myostatin and TGF-β induced the expression of TIEG1 and Smad7 mRNAs, but not TIEG2 mRNA, in proliferating C2C12 cells. When differentiating C2C12 myoblasts were stimulated by myostatin, TIEG1 mRNA was up-regulated at a late stage of differentiation. In contrast, TGF-β enhanced TIEG1 expression at an early stage. Overexpression of TIEG1 prevented the transcriptional activation of Smad by myostatin and TGF-β in both proliferating or differentiating C2C12 cells, but the expression of Smad2 and Smad7 mRNAs was not affected. Forced expression of TIEG1 inhibited myogenic differentiation but did not cause more inhibition than the empty vector in the presence of myostatin or TGF-β. These results demonstrate that TIEG1 is one possible feedback regulator of myostatin and TGF-β that prevents excess action in myoblasts.

本文言語英語
ページ(範囲)762-766
ページ数5
ジャーナルBiochemical and Biophysical Research Communications
393
4
DOI
出版ステータス出版済み - 3 19 2010
外部発表はい

All Science Journal Classification (ASJC) codes

  • 生物理学
  • 生化学
  • 分子生物学
  • 細胞生物学

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