Inhibition by dexamethasone of interleukin 13 production via glucocorticoid receptor-mediated inhibition of c-Jun phosphorylation

Noriyasu Hirasawa, Shinichiroh Izumi, Watchara Linwong, Kazuo Ohuchi

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

The antigen stimulation of RBL-2H3 cells induced interleukin 13 (IL-13) production, which was inhibited by the steroidal anti-inflammatory drug dexamethasone and by the c-Jun N-terminal kinase (JNK) inhibitor SP600125. Dexamethasone did not inhibit the antigen-induced phosphorylation of JNK but inhibited that of c-Jun. In a cell-free system, the phosphorylation of glutathione S-transferase-fused c-Jun by recombinant JNK was not inhibited by dexamethasone but was inhibited by the addition of recombinant glucocorticoid receptor (GR). These findings suggest that the inhibition of antigen-induced IL-13 production by dexamethasone is due to the GR-mediated inhibition of c-Jun phosphorylation induced by JNK.

Original languageEnglish
Pages (from-to)489-493
Number of pages5
JournalFEBS Letters
Volume554
Issue number3
DOIs
Publication statusPublished - 2003 Nov 20

Keywords

  • Dexamethasone
  • Glucocorticoid receptor
  • Interleukin 13
  • RBL-2H3 cell line
  • c-Jun
  • c-Jun N-terminal kinase

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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