Mechanisms of glucocorticoid receptor signaling during inflammation

Mech Ageing Dev. Oct-Nov 2004;125(10-11):697-706. doi: 10.1016/j.mad.2004.06.010.

Abstract

Glucocorticoids are among the most widely prescribed anti-inflammatory drugs. They act by binding to the glucocorticoid receptor (GR) that, upon activation, translocates to the nucleus and either stimulates or inhibits gene expression. GR inhibition of many proinflammatory response genes occurs through induction of the synthesis of anti-inflammatory proteins as well as through repression of proinflammatory transcription factors, such as nuclear factor-kappaB (NF-kappaB) or activator protein-1 (AP-1). In this review, we discuss the molecular mechanisms underlying GR inhibition of inflammatory responses, with an emphasis on repression of NF-kappaB and AP-1 and their respective signaling pathways.

Publication types

  • Review

MeSH terms

  • Animals
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / physiology*
  • Glucocorticoids / physiology*
  • Glucocorticoids / therapeutic use
  • Humans
  • Inflammation / drug therapy
  • Inflammation / physiopathology
  • NF-kappa B / metabolism
  • Receptors, Glucocorticoid / physiology*
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*
  • Transcription Factor AP-1 / metabolism

Substances

  • Glucocorticoids
  • NF-kappa B
  • Receptors, Glucocorticoid
  • Transcription Factor AP-1