Regulation of cyclooxygenase-2 expression in bovine chondrocytes in culture by interleukin 1alpha, tumor necrosis factor-alpha, glucocorticoids, and 17beta-estradiol

J Rheumatol. 1998 Jun;25(6):1146-53.

Abstract

Objective: To determine the effects of interleukin 1alpha (IL-1alpha), tumor necrosis factor-alpha (TNF-alpha), dexamethasone, and 17beta-estradiol on the expression of cyclooxygenase-1 (COX-1) and COX-2 in bovine chondrocytes.

Methods: Northern blot analysis was used to quantify COX-1 and COX-2 mRNA expression in primary cultures of bovine chondrocytes and prostaglandin production to evaluate COX activity.

Results: IL-1alpha and TNF-alpha increased the expression of COX-2. This effect was independent of de novo protein synthesis and dependent on increased mRNA stability in the case of IL-1alpha. Dexamethasone inhibited the effects of both cytokines. 17beta-estradiol inhibited COX-2 mRNA expression in basal conditions, but had no effect on COX-2 expression induced by cytokines. The specific COX-2 inhibitor compound NS 398 prevented the increase in prostaglandin E2 (PGE2) production induced by the cytokines. COX-1 levels remained stable with all treatments.

Conclusion: Increase in mRNA stability is a mechanism implicated in the induction of COX-2 by some cytokines. The effects of IL-1alpha and TNF-alpha on PGE2 production are mainly due to an increase in COX-2 activity as shown by the effect of compound NS 398. 17beta-estradiol inhibits COX-2 mRNA expression in basal conditions, suggesting that estrogens could be implicated in the control of cartilage metabolism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Northern
  • Cartilage, Articular / cytology
  • Cartilage, Articular / drug effects
  • Cartilage, Articular / enzymology
  • Cattle
  • Cells, Cultured
  • Chondrocytes / drug effects
  • Chondrocytes / enzymology*
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors / pharmacology
  • Cytokines / pharmacology*
  • Dexamethasone / pharmacology*
  • Dinoprostone / metabolism
  • Dose-Response Relationship, Drug
  • Estradiol / pharmacology*
  • Gene Expression Regulation, Enzymologic / drug effects*
  • Interleukin-1 / pharmacology
  • Isoenzymes / genetics*
  • Isoenzymes / metabolism
  • Nitrobenzenes / pharmacology
  • Prostaglandin-Endoperoxide Synthases / genetics*
  • Prostaglandin-Endoperoxide Synthases / metabolism
  • RNA, Messenger / metabolism
  • Recombinant Proteins / pharmacology
  • Sulfonamides / pharmacology
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors
  • Cytokines
  • Interleukin-1
  • Isoenzymes
  • Nitrobenzenes
  • RNA, Messenger
  • Recombinant Proteins
  • Sulfonamides
  • Tumor Necrosis Factor-alpha
  • N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide
  • Estradiol
  • Dexamethasone
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • Prostaglandin-Endoperoxide Synthases
  • Dinoprostone