Corticotropin-releasing hormone inhibits nuclear factor-kappaB pathway in human HaCaT keratinocytes

J Invest Dermatol. 2003 Dec;121(6):1496-9. doi: 10.1111/j.1523-1747.2003.12612.x.

Abstract

Treatment of human HaCaT keratinocytes with corticotropin-releasing hormone modulates cell proliferation and expression of inflammation markers. In this study we report that corticotropin-releasing hormone also inhibits nuclear factor-kappaB binding and transcriptional activity. Incubating cells in the absence of growth factors increased nuclear factor-kappaB activity; this effect was significantly attenuated by corticotropin-releasing hormone. Specifically, corticotropin-releasing hormone downregulated p50/p50 and p50/p65 dimers of nuclear factor-kappaB, diminished kappaB-driven CAT reporter gene activity and inhibited IkappaB-beta degradation. Moreover, corticotropin-releasing hormone inhibited the trans-cription of the nuclear factor-kappaB responsive genes, interleukin-2 and heat shock protein 90.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Blotting, Western
  • Cells, Cultured
  • Chloramphenicol O-Acetyltransferase / genetics
  • Corticotropin-Releasing Hormone / pharmacology*
  • Gene Expression / drug effects
  • Gene Expression / physiology
  • HSP90 Heat-Shock Proteins / genetics
  • Humans
  • I-kappa B Proteins / metabolism
  • Interleukin-2 / genetics
  • Keratinocytes / cytology
  • Keratinocytes / metabolism*
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / metabolism*
  • Signal Transduction / drug effects*
  • Signal Transduction / physiology

Substances

  • HSP90 Heat-Shock Proteins
  • I kappa B beta protein
  • I-kappa B Proteins
  • Interleukin-2
  • NF-kappa B
  • NFKBIA protein, human
  • NF-KappaB Inhibitor alpha
  • Corticotropin-Releasing Hormone
  • Chloramphenicol O-Acetyltransferase