Involvement of prostaglandins from rheumatoid synovium in inhibition of articular cartilage metabolism

Lippiello, Louis; Yamamoto, Kichizo; Robinson, Dwight R.; Mankin, Henry J.

doi:10.1002/art.1780210807

Cited by 82 publications

(22 citation statements)

References 19 publications

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“…Maybe this peptide acts as a messenger also in affecting the chondrocytes to inhibit their synthesis of proteoglycans. From other systems it has been reported that human rheumatoid tissue inhibits the synthesis of proteoglycans by cartilage [8,91, and it has been suggested that the inhibitory substance would be a prostaglandin ]8]. Prostaglandins have also been reported to inhibit glycosaminoglycan sulphation in both monolayer-and spinnercultured rabbit articular chondrocytes [10] as well as in pig costal cartilage [ 11].…”

Section: Discussionmentioning

confidence: 97%

Synthesis of articular cartilage proteoglycans by isolated bovine chondrocytes. Effect of autogenous conditioned synovial mediumin vitro

Klämfeldt

1984

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It was previously reported that bovine conditioned synovial medium (SM) has a catabolic activity on articular cartilage proteoglycans in an organ culture system. The question thus arose whether SM had an anabolic effect as well on articular cartilage proteoglycans. In this report it is shown that addition of autogenous SM to isolated bovine articular chondrocytes inhibited the synthesis of proteoglycans as measured by the incorporation of radiosulphate. Already after 4 hours an inhibition was seen in the pericellular (matrix) chondroitin sulphate (MA-CS) fraction, and in the culture medium chondroitin sulphate (CM-CS) fraction it was significant after 72 hours. When the synovial tissue was cultured with indomethacin (1.4 X 10(-5) mol/l) and this indo-SM was added to the chondrocyte cultures, the ability of the chondrocytes to incorporate [35S]sulphate was decreased further. It therefore seems evident that the products from the synovial tissue influences the behaviour of the chondrocyte in such a way that not only is the degradation enhanced but also the synthesis of cartilage proteoglycans is inhibited.

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Section: Discussionmentioning

confidence: 97%

Synthesis of articular cartilage proteoglycans by isolated bovine chondrocytes. Effect of autogenous conditioned synovial mediumin vitro

Klämfeldt

1984

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“…Naproxen may have inhibited cartilage erosion in the current study by interfering with the release of these catabolizing enzymes. Alternatively, prostaglandins, which are released by all three of these cell types, inhibit cartilage synthesis (23). Naproxen may have had a cartilage sparing action via its prostaglandin biosynthesis inhibitory activity.…”

Section: Discussionmentioning

confidence: 99%

Effects of naproxen on connective tissue changes in the adjuvant arthritic rat

Ackerman

Rooks

Shott

et al. 1979

Arthritis & Rheumatism

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The Freund's adjuvant‐injected rat shares a number of features with the arthritis patient, viz the presence of a proliferative synovitis, joint swelling, and cartilage and bone erosion. Naproxen, a prostaglandin synthetase inhibitor which is an effective antiinflammatory agent in laboratory animals and humans, was evaluated as an inhibitor of connective tissue destruction in this model by use of radiologic and histopathologic analyses. Sixteen days after rats were injected with Freund's complete adjuvant, marked joint swelling was noted. On day 17, vehicle or naproxen, 7 mg/kg/day, was administered orally. Twenty‐eight days later, vehicle‐treated animals demonstrated the following pathologic changes in their hindpaws: swelling, cartilage loss, large amounts of pannus within the joint spaces, osteoporosis, bone erosions, periosteal new bone formation, heterotopic ossification, and bony ankylosis. Rats treated 28 days with naproxen had significantly milder disease than the vehicle controls. The incidence of severe juxtaarticular bone destruction was 10/10 in the vehicle controls versus 2/10 of the drug‐treated group (P < 0.01). A comparable reduction in cartilage erosion, incidence of pannus, and new bone formation was noted in the drug‐treated group. These effects may relate to an inhibition of prostaglandin biosynthesis; prostaglandins have been shown to: 1) stimulate collagenase secretion from macrophages, 2) stimulate bone resorption in vivo and in vitro, and 3) diminish proteoglycan synthesis in cartilage.

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“…These compounds were, however, quite effective at blocking PGE, release in this organ culture system. Although prostaglandins have previously been reported to have an inhibitory effect on proteoglycan synthesis (26), the inability of the NSAIDs to antagonize the effects of IL-1 on proteoglycan metabolism at concentrations that totally block PGE, release indi- Table 3. Inhibition of the effects of recombinant human interleukin-lp (rHuIL-Ip) on proteoglycan metabolism by IL-I antiserum* cates that the actions of IL-1 on proteoglycan metabolism are not mediated through the production of prostaglandins.…”

Section: Discussionmentioning

confidence: 99%

Independent effects of interleukin‐1 on proteoglycan breakdown, proteoglycan synthesis, and prostaglandin E₂ release from cartilage in organ culture

Arner

Pratta

1989

Arthritis & Rheumatism

120

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Exposure of bovine nasal cartilage in culture to interleukin-1 (IL-1) leads to a time-and concentrationdependent stimulation of proteoglycan breakdown and prostaglandin E, (PGE,) release, and to inhibition of proteoglycan synthesis. The threshold levels of IL-1 required for initiating these effects were different, and IL-1 was 10 times more potent in inhibiting synthesis than in stimulating breakdown of proteoglycan. Kinetic studies indicated that the effects on proteoglycan metabolism occurred earlier (16-24 hours) than those for PGE, release (48 hours). Selective effects were observed with inhibitors. Nonsteroidal antiinflammatory drugs blocked PGE, production in response to IL-1, but had no effect on proteoglycan metabolism, and the antiarthritic drugs that blocked IL-1-stimulated breakdown augmented the inhibition of proteoglycan synthesis. We suggest that the effects of IL-1 on proteoglycan breakdown, proteoglycan synthesis, and PGE, release are mediated by independent post-receptor mechanisms.Interleukin-I (IL-I) is a monokine (1) that exhibits a number of immunologic effects (2-6) and modulates a variety of inflammatory functions relevant to rheumatic diseases, including the induction of fever (7), acute-phase proteins (8), and muscle proteolysis

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Involvement of prostaglandins from rheumatoid synovium in inhibition of articular cartilage metabolism

Cited by 82 publications

References 19 publications

Synthesis of articular cartilage proteoglycans by isolated bovine chondrocytes. Effect of autogenous conditioned synovial mediumin vitro

Synthesis of articular cartilage proteoglycans by isolated bovine chondrocytes. Effect of autogenous conditioned synovial mediumin vitro

Effects of naproxen on connective tissue changes in the adjuvant arthritic rat

Independent effects of interleukin‐1 on proteoglycan breakdown, proteoglycan synthesis, and prostaglandin E₂ release from cartilage in organ culture

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Involvement of prostaglandins from rheumatoid synovium in inhibition of articular cartilage metabolism

Cited by 82 publications

References 19 publications

Synthesis of articular cartilage proteoglycans by isolated bovine chondrocytes. Effect of autogenous conditioned synovial mediumin vitro

Synthesis of articular cartilage proteoglycans by isolated bovine chondrocytes. Effect of autogenous conditioned synovial mediumin vitro

Effects of naproxen on connective tissue changes in the adjuvant arthritic rat

Independent effects of interleukin‐1 on proteoglycan breakdown, proteoglycan synthesis, and prostaglandin E2 release from cartilage in organ culture

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Independent effects of interleukin‐1 on proteoglycan breakdown, proteoglycan synthesis, and prostaglandin E₂ release from cartilage in organ culture