Osmotic stress blocks NF-κB-dependent inflammatory responses by inhibiting ubiquitination of IκB

Wei Chun HuangFu, Kunihiro Matsumoto, Jun Ninomiya-Tsuji

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The inhibitory effects of hypertonic conditions on immune responses have been described in clinical studies; however, the molecular mechanism underlying this phenomenon has yet to be defined. Here we investigate osmotic stress-mediated modification of the NF-κB pathway, a central signaling pathway in inflammation. We unexpectedly found that osmotic stress could activate IκBα kinase but did not activate NF-κB. Osmotic stress-induced phosphorylated IκBα was not ubiquitinated, and osmotic stress inhibited interleukin 1-induced ubiquitination of IκBα and ultimately blocked expression of cytokine/chemokines. Thus, blockage of IκBα ubiquitination is likely to be a major mechanism for inhibition of inflammation by hypertonic conditions.

Original languageEnglish
Pages (from-to)5549-5554
Number of pages6
JournalFEBS Letters
Volume581
Issue number29
DOIs
Publication statusPublished - Dec 11 2007
Externally publishedYes

Keywords

  • Cytokine
  • Inflammation
  • NF-κB
  • Osmotic stress

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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