Glucocorticoids increase C/EBPbeta activity in the lung epithelium via phosphorylation

Biochem Biophys Res Commun. 2005 Aug 26;334(2):638-45. doi: 10.1016/j.bbrc.2005.06.146.

Abstract

Glucocorticoids are widely prescribed anti-inflammatory drugs used for the treatment of many inflammatory lung disorders. However, much still remains unknown about their molecular mechanisms of action. We have previously shown that glucocorticoid-induced transcription in the lung epithelial cell line NCI-H441 is mediated via C/EBP sites in the promoters of target genes, and is likely to involve the transcription factors C/EBPbeta and C/EBPdelta. Here, we report that C/EBPbeta is the most active C/EBP-factor in both human and mouse lung epithelium and that glucocorticoids induce DNA binding of C/EBPbeta in cultured primary mouse lung epithelial cells. Mechanistic studies in H441 cells revealed that glucocorticoids, acting via the glucocorticoid receptor, increase C/EBPbeta binding starting 10 min after stimulation. The mechanism is independent of de novo protein synthesis and involves phosphorylation of C/EBPbeta at Thr(235). Together this shows that glucocorticoids increase DNA-binding activity of C/EBPbeta via post-translational mechanism(s) involving phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CCAAT-Enhancer-Binding Protein-beta / metabolism*
  • Cell Line
  • Dexamethasone / administration & dosage*
  • Dose-Response Relationship, Drug
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / physiology
  • Glucocorticoids / administration & dosage*
  • Humans
  • Kinetics
  • Lung / cytology
  • Lung / drug effects
  • Lung / metabolism*
  • Mice
  • Phosphorylation / drug effects
  • Respiratory Mucosa / drug effects
  • Respiratory Mucosa / metabolism*

Substances

  • CCAAT-Enhancer-Binding Protein-beta
  • Glucocorticoids
  • Dexamethasone