The regulation of human MMP-13 by licofelone, an inhibitor of cyclo-oxygenases and 5-lipoxygenase, in human osteoarthritic chondrocytes is mediated by the inhibition of the p38 MAP kinase signalling pathway

Ann Rheum Dis. 2005 Jun;64(6):891-8. doi: 10.1136/ard.2004.026906. Epub 2004 Oct 21.

Abstract

Background: MMP-13 is one of the most important metalloproteases (MMP) involved in osteoarthritis. Licofelone, a novel dual inhibitor of cyclo-oxygenases (COX) and 5-lipoxygenase (5-LOX), can modulate MMP-13 production in human osteoarthritis chondrocytes.

Objective: To evaluate the impact of licofelone on MMP-13 expression/production, promoter, and major MAP kinase signalling pathways and transcription factors.

Methods: Human osteoarthritis chondrocytes were stimulated by interleukin 1beta (IL1beta) and treated with or without: licofelone (0.3, 1, or 3 mug/ml); NS-398 (10 muM; a specific COX-2 inhibitor); or BayX-1005 (10 muM; a specific 5-LOX inhibitor). MMP-13 synthesis was determined by specific enzyme linked immunosorbent assay, and expression by real time polymerase chain reaction. The effect of licofelone on the MMP-13 promoter was studied through transient transfection; dexamethasone (10(-7) M) was used as comparison. The effect on IL1beta induced MMP-13 signalling pathways was determined using specific ELISA for phosphorylated MAP kinases and transcription factors.

Results: Licofelone dose dependently inhibited the IL1beta stimulated production and expression of MMP-13. NS-398 and BayX-1005 had very little effect. Licofelone also inhibited MMP-13 transcription on each of the promoter constructs used. The licofelone inhibition was comparable to that obtained with dexamethasone. Licofelone had no effect on phosphorylated p44/42 or JNK1/2; however, it decreased phosphorylated c-jun and inhibited phosphorylated p38, CREB, and AP-1 activity.

Conclusions: Licofelone inhibited MMP-13 production under proinflammatory conditions on human osteoarthritis chondrocytes, through inhibition of the p38/AP-1 pathway and the transcription factor CREB. This may explain some of the mechanisms whereby licofelone exerts its positive effect on osteoarthritic changes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetates / pharmacology*
  • Aged
  • Cells, Cultured
  • Chondrocytes / drug effects*
  • Collagenases / biosynthesis
  • Collagenases / drug effects*
  • Collagenases / genetics
  • Cyclooxygenase Inhibitors / pharmacology
  • Dose-Response Relationship, Drug
  • Humans
  • Interleukin-1 / pharmacology
  • Lipoxygenase Inhibitors
  • MAP Kinase Signaling System / drug effects*
  • Matrix Metalloproteinase 13
  • Middle Aged
  • Osteoarthritis, Knee / enzymology*
  • Osteoarthritis, Knee / pathology
  • Promoter Regions, Genetic / drug effects
  • Pyrroles / pharmacology*
  • Signal Transduction / drug effects
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription, Genetic / drug effects

Substances

  • Acetates
  • Cyclooxygenase Inhibitors
  • Interleukin-1
  • Lipoxygenase Inhibitors
  • Pyrroles
  • Collagenases
  • MMP13 protein, human
  • Matrix Metalloproteinase 13
  • Tetradecanoylphorbol Acetate
  • licofelone