Ellies L G, Gupta A K, Aubin J E
MRC Group in Periodontal Physiology, University of Toronto, Canada.
Biochem Biophys Res Commun. 1992 Nov 16;188(3):1047-53. doi: 10.1016/0006-291x(92)91337-p.
Treatment of fetal rat calvarial cells with interleukin-1 alpha, tumor necrosis factor-alpha, transforming growth factor-beta 1, or group II phospholipase A2 inhibits the number of bone nodules formed in long-term cultures. These same mediators also inhibit the mineralization of fully developed bone nodules in a time and dose-dependent fashion. The pro-inflammatory cytokines interleukin-1 alpha and tumor necrosis factor-alpha cause a dose-dependent induction of rat calvarial cell phospholipase A2-II mRNA levels, suggesting that their effects on bone formation may be mediated indirectly by activation of this enzyme. In contrast, transforming growth factor-beta 1, which has more potent effects on bone formation than interleukin-1 alpha or tumor necrosis factor-alpha, suppresses basal levels of phospholipase A2-II mRNA, indicating a different mechanism of action for this cytokine.
用白细胞介素-1α、肿瘤坏死因子-α、转化生长因子-β1或II型磷脂酶A2处理胎鼠颅骨细胞，可抑制长期培养中形成的骨结节数量。这些相同的介质也以时间和剂量依赖的方式抑制完全发育的骨结节的矿化。促炎细胞因子白细胞介素-1α和肿瘤坏死因子-α导致大鼠颅骨细胞磷脂酶A2-II mRNA水平呈剂量依赖性诱导，表明它们对骨形成的影响可能通过该酶的激活间接介导。相比之下，对骨形成的影响比白细胞介素-1α或肿瘤坏死因子-α更强的转化生长因子-β1抑制磷脂酶A2-II mRNA的基础水平，表明该细胞因子的作用机制不同。
