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Combinatory responses of proinflamamtory cytokines on nitric oxide‐mediated function in mouse calvarial osteoblasts
Author(s) -
Park YoungGuk,
Kim KyungWoon,
Song KwonHo,
Lee JiMin,
Hong JeongJin,
Moon SungkKwon,
Kim CheorlHo
Publication year - 2009
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2008.09.012
Subject(s) - osteoblast , cytokine , tumor necrosis factor alpha , nitric oxide , alkaline phosphatase , medicine , stimulation , endocrinology , chemistry , sodium nitroprusside , transforming growth factor , microbiology and biotechnology , biology , in vitro , biochemistry , enzyme
Combinatory responses of proinflamamtory cytokines have been examined on the nitric oxide‐mediated function in cultured mouse calvarial osteoblasts. Interleukin‐1β (IL‐1β) and tumor necrosis factor‐α (TNF‐α) induced iNOS gene expression and NO production, although these actions were inhibited by L‐ N G‐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‐β (TGF‐β) decreased NO production stimulated by IL‐1β, TNF‐α and interferon‐γ (IFN‐γ). iNOS was expressed by mouse calvarial osteoblast cells after stimulation with IL‐1β, TNF‐α, and IFN‐γ. Incubation of mouse calvarial osteoblast cells with the cytokines inhibited growth and ALPase activity. However, TGF‐β‐treatment abolished these effects of IL‐1β, TNF‐α and IFN‐γ on growth inhibition and stimulation of ALPase in mouse calvarial osteoblast cells. In contrast, IL‐1β, TNF‐α, and IFN‐γ 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‐β is a negative regulator of the NO production stimulated by IL‐1β, TNF‐α and IFN‐γ.