Tumor necrosis factors α and β can stimulate bone resorption in cultured mouse calvariae by a Prostaglandin-independent mechanism
Tóm tắt
Human recombinant tumor necrosis factors α and β (TNF-α and TNF-β), at and above 1 ng/ml (≅ 70 pM), caused a dose- and time-dependent enhancement of 45Ca release from neonatal mouse calvarial bones in vitro. In addition, TNF-α and TNF-β (3–100 ng/ml) caused a dose-dependent stimulation of prostaglandin E2 (PGE2) formation in the calvarial bones. TNF-α also enhanced the biosynthesis of PGI2, as assessed by analysis of the stable breakdown product 6-keto-PGF1α. The stimulatory actions of TNF-α and TNF-β on PGE2 formation was maximal at 12 h. Indomethacin, flurbiprofen, and meclofenamic acid, three structurally unrelated nonsteroidal antiinflammatory drugs, abolished PGE2 biosynthesis induced by TNF-α and TNF-β (100 ng/ml). The 45Ca release stimulated by TNF-α and TNF-β (100 ng/ml), however, was only slightly reduced by indomethacin, flurbiprofen, and meclofenamic acid. The partial inhibitory effect of indomethacin on 45Ca release was seen over a wide range of TNF-α concentrations, without affecting the concentration producing half-maximal stimulatory response. TNF-α and TNF-β (100 ng/ml) stimulated bone matrix breakdown, as assessed by analysis of the release of 3H from bone prelabeled with [3H]proline. Also, the stimulatory effect of TNF-α and TNF-β on bone matrix degradation was partially reduced by indomethacin. Hydrocortisone (1 μM) and dexamethasone (0.1 μM) abolished TNF-α- and TNF-β-induced production of PGE2. In contrast to the cyclooxygenase inhibitors, the corticosteroids did not affect the stimulatory action by the cytokines on 45Ca release. These observations suggest that TNF-α and TNF-β can stimulate bone resorption in vitro by prostaglandin-independent mechanisms.
Từ khóa
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