Effects of various prostanoids on th in vitro metabolism of bovine articular chondrocytes

Mitrović, D; Lippiello, Louis; Gruson, F.; Aprile, F.; Mankin, Henry J.

doi:10.1016/0090-6980(81)90109-x

Cited by 29 publications

(10 citation statements)

References 12 publications

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“…Although aggrecan synthesis is reportedly reduced in chondrocytes and cartilage cultures in response to the addition of exogenous PGE2 [15,16], the PGE2 concentrations were much higher than the levels observed in rheumatoid synovial fluids (nanomolar range) [17]. In our hand, exogenous PGE2 inhibited proteoglycan synthesis over the concentration of 1 l, tM, measured by the conventional 35SO4 incorporation (data not shown).…”

Section: Discussioncontrasting

confidence: 74%

Interleukin-1 inhibits keratan sulfate production by rabbit chondrocytes: Possible role of prostaglandin E2

et al. 1995

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We investigated the importance of prostaglandin E2 (PGE2) release in interleukin-1 (IL-1)-induced inhibition of aggrecan synthesis by chondrocytes. Keratan sulfate (KS) production was measured in parallel with PGE2 release in chondrocytes. IL-1 inhibited KS production and stimulated PGE2 release. In the presence of PGE2, there was a dose-dependent decrease in baseline KS production. Indomethacin and dexamethasone partially blocked the IL-1-induced PGE2 release while KS production recovered. Our results suggest that IL-1 inhibits KS production, in part, by stimulating the release of PGE2.

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Section: Discussioncontrasting

confidence: 74%

Interleukin-1 inhibits keratan sulfate production by rabbit chondrocytes: Possible role of prostaglandin E2

et al. 1995

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“…During the destruction of cartilage, tissue pieces are phagocytosed by mononuclear cells. In the process, proteases, oxygen radicals, interleukins, and eicosanoids are released into the synovial fluid (17)(18)(19)(20)(21). Although concentrations of PG in synovial fluid under normal and disease conditions have been investigated (2-7), little is known about the source of tissues release of these eicosanoids.…”

mentioning

confidence: 99%

In vitro release of prostaglandins and leukotrienes from synovial tissue, cartilage, and bone in degenerative joint diseases

Wittenberg

Willburger

Kleemeyer

et al. 1993

Arthritis & Rheumatism

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Objective. To determine the major source of eicosanoid release in arthritic joint tissues and to examine the modulation of this release by indomethacin and diclofenac. Methods. Release of prostaglandin E2 (PGE2), 6‐keto‐PGF1α, leukotriene B4 (LTB4), and LTC4 was measured in supernatants of synovial tissue, cartilage, and bone incubates from patients with osteoarthritis, active rheumatoid arthritis (RA), inactive RA, and pseudogout. Radioimmunoassay (RIA) was used to determine the levels of the eicosanoids. Results. Addition of the divalent cation ionophore A23187 resulted in significant release of all eicosanoids measured from synovial tissue, but not from cartilage, cortical bone, or cancellous bone. PG release was significantly inhibited by the addition of indomethacin or diclofenac at either 10–5 moles/liter or 10–7 moles/liter. The amount of LTC4 released from cartilage and bone was only slightly above the detection limit of the RIA, whereas large amounts were released from synovial tissue. Neither indomethacin nor diclofenac had an effect on LTC4 release. LTC4 release from synovial tissue of patients with inactive RA was significantly decreased in comparison with the levels from synovial tissue of patients with the other joint diseases. There was no significant difference in PG release among patients in the various disease groups. Conclusion. Synovial tissue appears to be the major source of eicosanoids in synovial fluid. Indomethacin and diclofenac inhibit the release of PG, but not LT, from various joint tissues.

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“…Additionally, prostaglandins are known to alter cellular CAMP levels and act as signals for a variety of cellular activities (Dziak et al, 1983;Kurtz et al, 1974). Similarly, prostaglandins, especially of the E series, have been shown to alter cell cycle kinetics and therefore participate in the regulation of proliferation (Kurtz et al, 1974;Mitrovic et al, 1981). In preliminary studies, we observed that after pulse labeling of bone cell cultures with 3H-thymidine, only a relatively small percentage of the bone cell population could be shown to have labeled nuclei.…”

Section: Discussionmentioning

confidence: 85%

Multicellular tumor spheroid interactions with bone cells and bone

1985

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In vitro coculture techniques were used to study HSDM1C1 murine fibrosarcoma multicellular tumor spheroid (HSDM1C1-MTS) interactions with mouse calvarial bone cells having osteoblastic characteristics and mouse bone explants. HSDM1C1-MTS attached to confluent bone cell monolayers and their attachment rate was quantified. HSDM1C1-MTS interaction with bone cells was further demonstrated by the release of 3H-deoxyuridine from prelabeled bone cells during coculture with multicellular tumor spheroids. HSDM1C1-MTS-induced cytotoxicity was mimicked by the addition of 10(-5) M prostaglandin E2 (PGE2) to 3H-deoxyuridine-labeled bone cells. The effects of low (10(-9) M) and high (10(-5) M) concentrations of PGE2 on bone cell proliferation were also studied. Higher concentrations of PGE2 inhibited bone cell proliferation. HSDM1C1-MTS resorbed living explants in the presence of indomethacin, suggesting that other tumor cell products may also participate in bone resorption. HSDM1C1-MTS caused direct bone resorption as measured by the significantly elevated release of 45Ca from prelabeled, devitalized calvaria. However, the growth of a confluent bone cell layer on devitalized, 45Ca-prelabeled calvaria resulted in a significant reduction in the amount of 45Ca released subsequent to the seeding of HSDM1C1-MTS onto the explants. Bone cells at the bone surface may act as a barrier against invasion and tumor cell-mediated bone resorption. Violation of this cellular barrier is achieved, in part, by tumor cell products.

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Effects of various prostanoids on th in vitro metabolism of bovine articular chondrocytes

Cited by 29 publications

References 12 publications

Interleukin-1 inhibits keratan sulfate production by rabbit chondrocytes: Possible role of prostaglandin E2

Interleukin-1 inhibits keratan sulfate production by rabbit chondrocytes: Possible role of prostaglandin E2

In vitro release of prostaglandins and leukotrienes from synovial tissue, cartilage, and bone in degenerative joint diseases

Multicellular tumor spheroid interactions with bone cells and bone

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