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Insulin-like growth factor-I induces androgen receptor activation in differentiating C2C12 skeletal muscle cells

Hye Jin Kim1, Won Jun Lee

  • 1Department of Exercise Science, College of Health Sciences, Ewha Womans University, Seoul, Korea.

Molecules and Cells
|August 26, 2009
PubMed

Insights

Insulin-like growth factor-I (IGF-I) enhances androgen receptor (AR) expression and activation in skeletal muscle cells. This occurs through a ligand-independent pathway, promoting AR

Area of Science:

  • Muscle physiology
  • Endocrinology
  • Molecular biology

Background:

  • The role of Insulin-like Growth Factor-I (IGF-I) in regulating Androgen Receptor (AR) gene expression and activation in skeletal muscle is not fully understood.
  • Investigating IGF-I's effects on AR is crucial for understanding muscle growth and function.

Purpose of the Study:

  • To examine the effects of IGF-I on AR induction and activation in C2C12 skeletal muscle cells.
  • To determine if IGF-I can activate AR in a ligand-independent manner.

Main Methods:

  • C2C12 cells were treated with varying concentrations and durations of IGF-I.
  • Assessed AR expression, phosphorylation (pAR), and mRNA levels.
  • Utilized confocal microscopy for AR nuclear localization and electrophoretic mobility shift assay (EMSA) for DNA binding activity.

Main Results:

  • IGF-I treatment dose- and time-dependently increased total AR and phosphorylated AR (Ser 213) levels.
  • AR mRNA expression, along with AR target genes (skeletal alpha-actin, myogenin), were significantly upregulated by IGF-I.
  • IGF-I promoted AR nuclear localization and enhanced AR DNA binding activity in a ligand-independent manner.

Conclusions:

  • IGF-I stimulates AR expression and activation in differentiating C2C12 mouse skeletal muscle cells.
  • This activation occurs via a ligand-independent mechanism, suggesting a novel pathway for AR regulation in muscle.

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