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Related Experiment Videos

Altered gene expression in steroid-treated denervated muscle.

M M Rich1, S D Kraner, R L Barchi

  • 1Department of Neurology, Emory University School of Medicine, WMB Suite 6000, 1639 Pierce Drive, Atlanta, GA 30322, USA. mmrich@emory.edu

Neurobiology of Disease
|December 22, 1999
PubMed
Summary

High-dose corticosteroids combined with denervation in rats led to increased expression of the embryonic sodium channel isoform (SkM2) in skeletal muscle, contributing to electrical inexcitability. This suggests a role for SkM2 in steroid-induced myopathy.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Physiology

Background:

  • Corticosteroids and denervation can cause skeletal muscle electrical inexcitability.
  • This condition resembles acute quadriplegic myopathy in humans.

Purpose of the Study:

  • To investigate if altered gene transcription underlies the electrical inexcitability in steroid-denervated skeletal muscle.
  • To quantify mRNA levels of specific sodium and chloride channel isoforms.

Main Methods:

  • RNase protection assays were used to measure mRNA levels.
  • Skeletal muscle from control, denervated, steroid-innervated, and steroid-denervated rats were analyzed.
  • Levels of adult (SkM1) and embryonic (SkM2) sodium channel isoforms and chloride channel 1 (CLC-1) mRNA were quantified.

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Main Results:

  • Adult sodium channel (SkM1) mRNA levels were largely unaffected by denervation or steroid treatment.
  • Embryonic sodium channel (SkM2) mRNA levels increased with both denervation and corticosteroid treatment.
  • A synergistic increase in SkM2 mRNA was observed in steroid-denervated muscle.
  • Chloride channel 1 (CLC-1) mRNA levels decreased following denervation.
  • Changes in myogenin and glucocorticoid receptor mRNA did not explain SkM2 upregulation.

Conclusions:

  • The study identifies a significant upregulation of the embryonic sodium channel isoform (SkM2) in steroid-denervated skeletal muscle.
  • This upregulation of SkM2 mRNA is a key molecular event potentially contributing to the observed electrical inexcitability.
  • Further research is needed to fully elucidate the mechanisms behind SkM2 upregulation in this model.