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Use of artificial androgen receptor coactivators to alter myoblast proliferation

Cara L Benjamin1, Guido Jenster, Jorge A Piedrahita

  • 1Department of Veterinary Anatomy and Public Health, Texas A&M University, College Station, TX 77843-4458, USA.

The Journal of Steroid Biochemistry and Molecular Biology
|July 28, 2004
PubMed

Insights

Mutated androgen receptors (AR) enhance muscle cell growth and differentiation. These modified ARs show altered specificity, responding to both androgens and estrogens, offering new insights into muscle development and androgen action.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Muscle Physiology

Background:

  • Skeletal muscle is a known target for androgens, mediated by the androgen receptor (AR).
  • Understanding AR action is crucial for muscle growth and development.
  • Previous research has focused on wild-type AR function in muscle tissue.

Purpose of the Study:

  • To investigate the effects of mutated androgen receptors (AR) on skeletal muscle cells.
  • To determine the specificity and cellular responses of engineered AR variants.
  • To explore the potential of mutated ARs as tools for studying androgen-mediated muscle growth.

Main Methods:

  • Development of mutated androgen receptors (AR) with alterations in the ligand-binding and transactivating domains.
  • Reporter assays in HeLa cells to assess AR specificity and response to androgens.
  • Transfection of wild-type and mutant AR into mouse and rat myoblast cell lines.
  • Analysis of cell proliferation and differentiation following treatment with testosterone and estrogen.

Main Results:

  • Mutations in the AR ligand-binding domain, particularly H865Y, decreased specificity and increased response to androgens.
  • Transfected mutant ARs increased reporter gene expression in myoblasts, similar to HeLa cell results.
  • Overexpression of wild-type and mutant AR in myoblasts led to increased proliferation and differentiation compared to endogenous AR.
  • Mutant AR-expressing cells responded to estrogen similarly to testosterone, indicating altered hormone sensitivity.

Conclusions:

  • Mutated androgen receptors can act as artificial coactivators, up-regulating androgen-responsive genes.
  • These engineered ARs provide a valuable tool for understanding androgen interactions in muscle growth.
  • The altered specificity of mutant ARs offers new avenues for research into hormone signaling in skeletal muscle.

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