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首页> 外文期刊>Cellular Signalling >Leukemia inhibitory factor enhances bFGF-induced IL-6 synthesis in osteoblasts: Involvement of JAK2/STAT3
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Leukemia inhibitory factor enhances bFGF-induced IL-6 synthesis in osteoblasts: Involvement of JAK2/STAT3

机译：白血病抑制因子增强成骨细胞中bFGF诱导的IL-6合成：JAK2 / STAT3的参与

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We previously showed that basic fibroblast growth factor (bFGF) stimulates release of vascular endothelial growth factor (VEGF) and synthesis of interleukin-6 (IL-6) in osteoblast-like MC3T3-E1 cells. In the present study, we investigated the effects of leukemia inhibitory factor (LIF) on the release of VEGF and IL-6 in these cells. LIF did not affect the bFGF-stimulated VEGF release. On the contrary, LIF, which alone had little effect on IL-6 release, significantly enhanced the bFGF-stimulated IL-6 release. The amplifying effect of LIF on the IL-6 release was dose dependent in the range between 0.01 and 10 ng/ml. AG490, an inhibitor of JAK2, suppressed the amplifying effect of LIF. LIF induced the phosphorylation of STAT3. AG490 inhibited the LIF-induced STAT3 phosphorylation. Taken together, our results strongly suggest that LIF enhances bFGF-stimulated IL-6 synthesis via JAK2/STAT3 pathway in osteoblasts. (C) 2002 Elsevier Science Inc. All rights reserved. [References: 26]
机译：我们以前显示碱性成纤维细胞生长因子（bFGF）刺激血管内皮生长因子（VEGF）的释放和成骨细胞样MC3T3-E1细胞中白介素6（IL-6）的合成。在本研究中，我们研究了白血病抑制因子（LIF）对这些细胞中VEGF和IL-6释放的影响。 LIF不影响bFGF刺激的VEGF释放。相反，仅对IL-6释放几乎没有影响的LIF显着增强了bFGF刺激的IL-6释放。 LIF对IL-6释放的放大作用取决于剂量，范围为0.01到10 ng / ml。 AGK，JAK2的抑制剂，抑制了LIF的放大作用。 LIF诱导STAT3磷酸化。 AG490抑制LIF诱导的STAT3磷酸化。两者合计，我们的结果强烈表明LIF通过成骨细胞中JAK2 / STAT3途径增强bFGF刺激的IL-6合成。 （C）2002 Elsevier Science Inc.保留所有权利。 [参考：26]

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