Differential regulation of IGF-I and IGF-II gene expression in skeletal muscle cells

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• 作者：Shuang Jiao (1)
  Hongxia Ren (2)
  Yun Li (1)
  Jianfeng Zhou (1)
  Cunming Duan (2)
  Ling Lu (1)
  
• 关键词：Akt ; IGF ; MAPK ; mTOR ; Myogenesis
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2013
• 出版时间：2 - January 2013
• 年：2013
• 卷：373
• 期：1
• 页码：107-113
• 全文大小：243KB
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• 作者单位：Shuang Jiao (1)
  Hongxia Ren (2)
  Yun Li (1)
  Jianfeng Zhou (1)
  Cunming Duan (2)
  Ling Lu (1)
  
  1. Key Laboratory of Marine Drugs, Ministry of Education, School of Medicine and Pharmacy, Ocean University of China, Qingdao, 266003, People鈥檚 Republic of China
  2. Department of Molecular, Cellular, and Developmental Biology, University of Michigan, Ann Arbor, MI, 48109, USA
  
• ISSN：1573-4919

文摘

Insulin-like growth factor (IGF)-I and IGF-II play major roles in the regulation of skeletal muscle growth and differentiation, and both are locally expressed in muscle cells. Recent studies have demonstrated that IGF-II up-regulates its own gene expression during myogenesis and this auto-regulatory loop is critical for muscle differentiation. How local IGF-I is regulated in this process is unclear. Here, we report that while IGF-II up-regulated its own gene expression, it suppressed IGF-I gene expression during myogenesis. These opposite effects of IGF-II on IGF-I and IGF-II genes expression were time dependent and dose dependent. It has been shown that IGFs activate the PI3K-Akt-mTOR, p38 MAPK, and Erk1/2 MAPK pathways. In myoblasts, we examined their role(s) in mediating the opposite effects of IGF-II. Our results showed that both the PI3K-Akt-mTOR and p38 MAPK pathways played critical roles in increasing IGF-II mRNA expression. In contrast, mTOR was required for down-regulating the IGF-I gene expression by IGF-II. In addition, Akt, Erk1/2 MAPK, and p38 MAPK pathways were also involved in the regulation of basal levels of IGF-I and IGF-II genes during myogenesis. These findings reveal a previously unrecognized negative feedback mechanism and extend our knowledge of IGF-I and IGF-II gene expression and regulation during myogenesis.