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Oestrogens inhibit interleukin 1beta-mediated nitric oxide synthase expression in articular chondrocytes through

Pascal Richette1, Marie-France Dumontier, Khadija Tahiri

  • 1INSERM UMR-747, Universite Paris Descartes, UFR Biomedicale, Paris, France.

Annals of the Rheumatic Diseases
|October 28, 2006
PubMed
Abstract

Insights

Oestrogen receptor alpha (ERalpha) in chondrocytes inhibits interleukin-1beta-induced nitric oxide production. This occurs by reducing inducible nitric oxide synthase (iNOS) gene expression via decreased NF-kappaB p65 DNA binding and nuclear translocation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Interleukin-1beta (IL-1beta) is a pro-inflammatory cytokine implicated in cartilage degradation.
  • Oestrogen receptors, particularly oestrogen receptor alpha (ERalpha), play roles in various cellular processes.
  • The interaction between oestrogens and inflammatory pathways in chondrocytes is not fully understood.

Purpose of the Study:

  • To investigate ERalpha presence and function in IL-1beta-treated rabbit articular chondrocytes.
  • To elucidate the mechanisms by which 17beta-oestradiol (E2) affects IL-1beta-induced inducible nitric oxide synthase (iNOS) expression.

Main Methods:

  • Immunocytochemistry and reporter gene assays for ERalpha functionality.
  • Reporter gene assays and immunoblotting for iNOS expression and production.
  • Griess reaction for nitric oxide (NO) production.
  • Electrophoretic mobility shift assay (EMSA)-ELISA for transcription factor DNA-binding.
  • Immunocytochemistry for p65 nuclear translocation.

Main Results:

  • ERalpha was identified in chondrocyte nuclei and was functional.
  • IL-1beta treatment caused partial ERalpha cytoplasmic diffusion and impaired transactivation.
  • E2, tamoxifen, and raloxifene inhibited IL-1beta-induced NO production and iNOS protein expression.
  • E2 reduced iNOS transcription, p65 DNA-binding capacity, and p65 nuclear translocation.

Conclusions:

  • Oestrogens and IL-1beta exhibit reciprocal antagonism in chondrocytes.
  • Oestrogens decrease cytokine-dependent NO production by transcriptionally inhibiting iNOS.
  • This inhibitory effect is mediated by selective inhibition of p65 DNA binding and nuclear translocation.

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