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Effect of burn injury on glucocorticoid receptor binding activity in rat muscle

Xiaoyan Sun1, David R Fischer, Mingyan Yang

  • 1Department of Surgery, University of Cincinnati, Cincinnati, Ohio, and Shriners Hospitals for Children, Cincinnati, OH 45267-0558, USA. sunxn@email.uc.edu

The Journal of Surgical Research
|March 12, 2004
PubMed

Insights

Burn injury increases muscle proteolysis, mediated by glucocorticoids (GCs). This study found burn injury enhances GC receptor (GR) binding activity in skeletal muscle by increasing receptor numbers, not affinity.

Area of Science:

  • Physiology
  • Molecular Biology
  • Endocrinology

Background:

  • Burn injury triggers muscle proteolysis and upregulates proteolytic pathways.
  • Glucocorticoids (GCs) are key mediators of burn-induced muscle wasting (cachexia).
  • Mechanisms of GC action in burn injury response are not fully understood.

Purpose of the Study:

  • To investigate the impact of burn injury on glucocorticoid receptor (GR) hormone binding activity in skeletal muscle.
  • To elucidate the molecular mechanisms underlying GC action post-burn injury.

Main Methods:

  • Examined GR hormone binding activity in extensor digitorum longus (EDL) and soleus muscles post-burn injury.
  • Utilized Scatchard plot analysis to assess receptor binding characteristics.
  • Employed Western blot to analyze GR/heat shock protein 90 (HSP90) heterocomplex and GR protein levels.
  • Assessed the effect of the GR antagonist RU 38486.

Main Results:

  • Burn injury significantly increased GR hormone binding activity in EDL and soleus muscles.
  • Scatchard analysis indicated an increase in the number of GR binding sites, with no change in receptor affinity for GCs.
  • Western blot suggested GR/HSP90 dissociation or increased GR protein levels contribute to enhanced binding.
  • RU 38486 administration blocked the burn-induced increase in GR hormone binding activity.

Conclusions:

  • Burn injury enhances glucocorticoid receptor (GR) hormone binding activity in skeletal muscle primarily by increasing receptor number.
  • The findings suggest a positive regulatory role of GCs on GR binding activity following burn injury.
  • Understanding these mechanisms is crucial for addressing burn-related muscle catabolism.

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