The role of the human synovial fibroblast in monosodium urate crystal-induced synovitis

F. M. Wigley; I. T. Fine; D. S. Newcombe

The role of the human synovial fibroblast in monosodium urate crystal-induced synovitis

F. M. Wigley, I. T. Fine, D. S. Newcombe

School of Medicine

Research output: Contribution to journal › Article › peer-review

13 Scopus citations

Abstract

Human synovial fibroblasts (HSF) have been cultured to identify and quantitate arachidonate metabolites released after exposure to monosodium urate (MSU) crystals. These crystals caused a significant release of PGE₂ and 6-keto-PGF₁(α). Media lactate dehydrogenase levels from MSU-exposed HSF were equal to controls. Serum was required for the increase in metabolite release. Indomethacin and dexamethasone inhibited metabolite release, whereas colchicine increased metabolite release. MSU (1 mg/ml) released hydroxyeicosatetraenoic acids (HETE) from HSF whereas 20-fold higher doses were required to release these metabolites from human polymorphonuclear leukocytes. Colchicine increased but lipoxygenase inhibitors decreased HETE synthesis. Arachidonate, metabolites from HSF may contribute to the pathogenesis of crystal-provoked synovitides.

Original language	English (US)
Pages (from-to)	602-611
Number of pages	10
Journal	Journal of Rheumatology
Volume	10
Issue number	4
State	Published - Dec 1 1983

ASJC Scopus subject areas

Rheumatology
Immunology and Allergy
Immunology

Cite this

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abstract = "Human synovial fibroblasts (HSF) have been cultured to identify and quantitate arachidonate metabolites released after exposure to monosodium urate (MSU) crystals. These crystals caused a significant release of PGE2 and 6-keto-PGF1(α). Media lactate dehydrogenase levels from MSU-exposed HSF were equal to controls. Serum was required for the increase in metabolite release. Indomethacin and dexamethasone inhibited metabolite release, whereas colchicine increased metabolite release. MSU (1 mg/ml) released hydroxyeicosatetraenoic acids (HETE) from HSF whereas 20-fold higher doses were required to release these metabolites from human polymorphonuclear leukocytes. Colchicine increased but lipoxygenase inhibitors decreased HETE synthesis. Arachidonate, metabolites from HSF may contribute to the pathogenesis of crystal-provoked synovitides.",

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The role of the human synovial fibroblast in monosodium urate crystal-induced synovitis

Abstract

ASJC Scopus subject areas

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