Fibroblast growth factor enhances the interleukin-1-mediated chondrocytic protease release

Phadke, Kalindi

doi:10.1016/0006-291x(87)90295-6

Cited by 39 publications

(15 citation statements)

References 14 publications

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“…The influence of IL-1 on PDGF receptor number, however, was not examined. Basic fibroblast growth factor was shown to potentiate neutral proteinase production by RAC exposed to IL-1 (49)(50)(51) and to increase the IL-1R number, which was mRNA-dependent (50,511. In contrast to the effects of IL-1 on PDGF receptor number reported here, the number of high-affinity bFGF receptors on RAC was down-regulated by IL-1 (51).…”

Section: Discussionmentioning

confidence: 98%

Platelet‐derived growth factor potentiates cellular responses of articular chondrocytes to interleukin‐1

Smith

Justen

Sam

et al. 1991

Arthritis & Rheumatism

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Recombinant human interleukin-la (IL-la) induced a time-dependent (0-72 hours) and concentration-dependent (0.01-10 ng/ml) production of metalloproteinases (collagenase, gelatinase, stromelysin) and prostaglandin E, (PGE,) in rabbit articular chondrocytes (RAC). Exposure of RAC to recombinant human plateletderived growth factor homodimer BB (PDGF-BB; 2-200 ng/ml) in the presence of stimulatory and substimulatory concentrations of IL-la resulted in a marked augmentation of metalloproteinase and PGE, production. PDGF-BB exerted no agonist effects on RAC responsiveness. PDGF-BB up-regulated the number of IL-1 receptors per chondrocyte but had no effect on receptor affinity. Cycloheximide and actinomycin D caused a concentrationdependent suppression of the PDGF-BB-mediated potentiation of radiolabeled IL-la binding to RAC and cell responsiveness to IL-la. Similarly, IL-1 increased the number of PDGF receptors on RAC without changing receptor affiity. These data are discussed within the context of cytokine-growth factor interactions as components of the pathogenesis of arthritic diseases.Articular cartilage erosion and resorption of subchondral bone in inflammatory joint disease is caused by matrix metalloproteinases (MMP) and prostanoids released from the proliferative synovial lesion that is in contact with the cartilage surface (1,2). The inflamed synovium is composed of heterogenous cell populations which produce a broad spectrum of cytokines and growth factors, which, in turn, stimulate MMP and prostaglandin E, (PGE,) production by synovial fibroblasts (3-5). The occurrence of interleukin-1 (IL-1) (6), tumor necrosis factor a (TNFa) (7), platelet-derived growth factor (PDGF) (8), and IL-6 (9) in arthritic synovial fluid implies a pathogenic role(s) for these factors.IL-1 is a 17-kd polypeptide that is produced by rheumatoid synovial tissue (10,ll) and chondrocytes (12). Synovial cells (13) and chondrocytes (14,15) express IL-1 receptors and produce MMP and PGE, in response to 4,[15][16][17][18][19]. A major role of IL-I in the pathogenesis of arthritic diseases is supported by reports of IL-I stimulating B and T lymphocyte proliferation, a febrile response, bone resorption, and the production of acute-phase reactants (20). PDGF is produced by macrophages, platelets, and endothelial cells (21), which are components of the inflamed synovium. PDGF is a chemoattractant for monocytes, fibroblasts, and neutrophils (22) and is mitogenic for fibroblasts, vascular smooth muscle cells, and chondrocytes (21).Since it is unlikely that tissue destruction in rheumatoid arthritis is mediated by any one cytokine and/or growth factor, synergistic interactions between MATERIALS AND METHODSChondrocyte culture. Confluent monolayer cultures of rabbit articular chondrocytes (RAC) were used throughout this study. The monolayer cultures were obtained from single-cell suspensions of chondrocytes isolated from the articular cartilage of the knee joints of New Zealand white rabbits, as described by Chin and Lin (18). Briefly, cartilage t...

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Section: Discussionmentioning

confidence: 98%

Platelet‐derived growth factor potentiates cellular responses of articular chondrocytes to interleukin‐1

Smith

Justen

Sam

et al. 1991

Arthritis & Rheumatism

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“…Epidermal growth factor was also reported to have IL-1 -induced collagenase-production-enhancing activity in periosteal explants from rabbit calvariae (Zee et al, 1993), but purified epidermal growth factor did not have such activity in our rat synovial fibroblasts. Some authors have reported that fibroblast growth factor (FGF) markedly enhanced IL-I-induced production of PGE,, collagenase or other proteases in chondrocytes (Phadke, 1987;Bandara et al, 1989;Chandrasekhar and Harvey, 1992). In our system using cultured synovial cells, recombinant FGF showed a significant enhancing activity.…”

Section: Discussionmentioning

confidence: 99%

A Factor Derived from Polymorphonuclear Leukocytes Enhances Interleukin‐1‐Induced Synovial Cell Collagenase and Prostaglandin E₂ Production in Rats

Hashida

Chiba

Horizoe

et al. 1996

European Journal of Biochemistry

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We found that short-term culture medium and homogenate of casein-induced rat peritoneal polymorphonuclear leukocytes (PMN) markedly induced collagenase and prostaglandin E, (PGE,) production by normal rat synovial cells and these effects were abrogated by anti-(rat interleukin-la) (IL-la) polyclonal antibodies. However, collagenase activity and PGE, induced by recombinant rat IL-la were less than those induced by rat PMN culture medium. It was also proved by radioimmunoassay that rat PMN culture medium contains a relatively small amount of IL-la. The introduction of IL-la-deleted PMN culture medium and recombinant rat IL-la together into the synovial cell culture system revealed that IL-ladeleted PMN culture medium has a significant enhancing activity on IL-la-induced synovial cell collagenase and PGE, production. This new factor, which was shown to be a negatively charged protein of about 80 kDa, may have important roles in connective tissue destruction and chronic inflammation in diseases such as rheumatoid arthritis.

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“…TGFP decreases protease secretion and increases protease inhibitor secretion in endothelial cells [147], and thus antagonizes HBGF-induced protease production. In contrast, 1L-1 is synergistic with bFGF in inducing protease production in chondrocytes [94].…”

Section: Synergism With Other Mitogensmentioning

confidence: 97%

Clinical applications of heparin‐binding growth factors

Lobb

1988

Eur J Clin Investigation

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Fibroblast growth factor enhances the interleukin-1-mediated chondrocytic protease release

Cited by 39 publications

References 14 publications

Platelet‐derived growth factor potentiates cellular responses of articular chondrocytes to interleukin‐1

Platelet‐derived growth factor potentiates cellular responses of articular chondrocytes to interleukin‐1

A Factor Derived from Polymorphonuclear Leukocytes Enhances Interleukin‐1‐Induced Synovial Cell Collagenase and Prostaglandin E₂ Production in Rats

Clinical applications of heparin‐binding growth factors

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Fibroblast growth factor enhances the interleukin-1-mediated chondrocytic protease release

Cited by 39 publications

References 14 publications

Platelet‐derived growth factor potentiates cellular responses of articular chondrocytes to interleukin‐1

Platelet‐derived growth factor potentiates cellular responses of articular chondrocytes to interleukin‐1

A Factor Derived from Polymorphonuclear Leukocytes Enhances Interleukin‐1‐Induced Synovial Cell Collagenase and Prostaglandin E2 Production in Rats

Clinical applications of heparin‐binding growth factors

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A Factor Derived from Polymorphonuclear Leukocytes Enhances Interleukin‐1‐Induced Synovial Cell Collagenase and Prostaglandin E₂ Production in Rats