Abstract
Combinatory responses of proinflamamtory cytokines have been examined on the nitric oxide-mediated function in cultured mouse calvarial osteoblasts. Interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) induced iNOS gene expression and NO production, although these actions were inhibited by L-NG-monomethylarginine (L-NMMA) and decreased alkaline phosphatase (ALPase) activity. Furthermore, NO donors, sodium nitroprusside (SNP) and NONOate dose-dependently elevated ALPase activity. In contrast, transforming-growth factor-beta (TGF-beta) decreased NO production stimulated by IL-1beta, TNF-alpha and interferon-gamma (IFN-gamma). iNOS was expressed by mouse calvarial osteoblast cells after stimulation with IL-1beta, TNF-alpha, and IFN-gamma. Incubation of mouse calvarial osteoblast cells with the cytokines inhibited growth and ALPase activity. However, TGF-beta-treatment abolished these effects of IL-1beta, TNF-alpha and IFN-gamma on growth inhibition and stimulation of ALPase in mouse calvarial osteoblast cells. In contrast, IL-1beta, TNF-alpha, and IFN-gamma exerted growth-inhibiting effects on mouse calvarial osteoblast cells which were partly NO-dependent. The results suggest that NO may act predominantly as a modulator of cytokine-induced effects on mouse calvarial osteoblast cells and TGF-beta is a negative regulator of the NO production stimulated by IL-1beta, TNF-alpha and IFN-gamma.
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