Heat shock protects L6 myotubes from catabolic effects of dexamethasone and prevents downregulation of NF-κB

Guangju Luo, Xiaoyan Sun, Eric Hungness, Per Olof Hasselgren*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

Glucocorticoids are the most important mediator of muscle cachexia in various catabolic conditions. Recent studies suggest that the transcription factor NF-κB acts as a suppressor of genes in the ubiquitin-proteasome proteolytic pathway and that glucocorticoids increase muscle proteolysis by downregulating NF-κB activity. The heat shock (stress) response, characterized by the induction of heat shock proteins, confers a protective effect against a variety of harmful stimuli. In the present study, we tested the hypothesis that the heat shock response protects muscle cells from the catabolic effects of dexamethasone and prevents downregulation of NF-κB. Cultured L6 myotubes were subjected to heat shock (43°C for 1 h) followed by recovery at 37°C for 1 h. Thereafter, cells were treated for 6 h with 1 μM dexamethasone, during which period protein degradation was measured as release of TCA-soluble radioactivity from proteins that had been prelabeled with [3H]tyrosine. Heat shock resulted in increased protein and mRNA levels for heat shock protein 70. The increase in protein degradation induced by dexamethasone was prevented in cells expressing the heat shock response. In the same cells, dexamethasone-induced downregulation of NF-κB DNA binding activity was blocked. The present results suggest that the heat shock response may protect muscle cells from the catabolic effects of dexamethasone and that this effect of heat shock may be related to inhibited downregulation of NF-κB activity.

Original languageEnglish (US)
Pages (from-to)R1193-R1200
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume281
Issue number4 50-4
DOIs
StatePublished - 2001

Keywords

  • Heat shock protein 70
  • Muscle cachexia
  • Nuclear factor-κB
  • Proteolysis

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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