1987
DOI: 10.1007/bf01966506
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Interleukin-1 induces chondrocyte protease production: The development of collagenase inhibitors

Abstract: Supernatants from the P388D1 macrophage cell line as well as human interleukin-1 (IL-1) stimulated primary rabbit articular chondrocytes to produce collagen- (C-ase) and proteoglycan- (PG-ase) degrading proteases. The P388D1 derived factor had a molecular weight of 16,000-20,000 and a pI of 4.5-5.0. Both protease activities were metal dependent and inhibited by EDTA, phenanthroline, and alpha 2-macroglobulin but not by PMSF, TLCK, pepstatin, or alpha 1-antitrypsin. Size exclusion chromatography indicated the m… Show more

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Cited by 6 publications
(2 citation statements)
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“…Addition of IL-1 to articular cartilage induces the degradation of the cartilage matrix and results in the release of proteoglycan and decrease of the synthesis of proteoglycan and glycosaminoglycan (4,16). The effect of IL-1 on human, bovine, and rabbit articular chondrocytes results in the release of hyaluronate binding region (24,27) and an increase in collagenase and neutral proteoglycanase activity (1,24,28). In studies of human IL-1 effects on bovine nasal and articular cartilage (31), addition of the protein synthesis inhibitor cycloheximide blocked IL-1 stimulation of proteoglycan release, whereas the addition of hydrocortisone had little or no effect on PG release (31).…”
Section: Discussionmentioning
confidence: 99%
“…Addition of IL-1 to articular cartilage induces the degradation of the cartilage matrix and results in the release of proteoglycan and decrease of the synthesis of proteoglycan and glycosaminoglycan (4,16). The effect of IL-1 on human, bovine, and rabbit articular chondrocytes results in the release of hyaluronate binding region (24,27) and an increase in collagenase and neutral proteoglycanase activity (1,24,28). In studies of human IL-1 effects on bovine nasal and articular cartilage (31), addition of the protein synthesis inhibitor cycloheximide blocked IL-1 stimulation of proteoglycan release, whereas the addition of hydrocortisone had little or no effect on PG release (31).…”
Section: Discussionmentioning
confidence: 99%
“…The contemporary treatment of OA is aimed at slowing disease progression through alteration of pathobiological pathways. Interleukin-1 (IL-1) has been commonly implicated as a key mediator in the progression of OA (18,23,24,40); it inhibits proteoglycan and type-II collagen synthesis (4,8,20) and promotes cartilage matrix degradation (14,21). Specifically, IL-1 'down-regulates' the expression of genes encoding structural matrix molecules, while simultaneously 'up-regulating' the expression of matrix degradative enzymes in vitro (26).…”
Section: Introductionmentioning
confidence: 99%