LPS Promotes Pre-osteoclast Activity by Up-regulating CXCR4 via TLR-4
LPS Promotes Pre-osteoclast Activity by Up-regulating CXCR4 via TLR-4
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DOI：
10.1177/0022034510379019
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发表时间：
2011-02-01
影响因子：
7.6
通讯作者：
Ren, Y.
中科院分区：
文献类型：
--
作者：
Xing, Q.;de Vos, P.;Ren, Y.
脂多糖(LPS)是炎症性骨丢失的重要致病因素。然而，对所涉及的机制的了解有限。SDF-1/CXCR4(基质衍生因子-1及其独特的趋化因子受体)轴在脂多糖诱导的骨丢失中的作用还没有研究。本研究的目的是探讨SDF-1/CXCR4轴在脂多糖刺激的炎症性骨丢失中的作用。结果表明，内毒素不影响成骨细胞SDF-1/CXCR4的表达，但通过Toll样受体4上调破骨前细胞中CXCR4的表达，从而促进破骨前细胞的迁移。此外，内毒素促进RANKL诱导的破骨细胞分化部分是通过上调CXCR4来实现的。综上所述，本研究首次证实了内毒素刺激下破骨前细胞CXCR4的表达上调参与了内毒素诱导的骨吸收。
Lipopolysaccharide (LPS) has been shown to be a prominent pathogenic factor in inflammatory bone loss. However, knowledge of the mechanisms involved is limited. The role of the SDF-1/CXCR4 (Stromal-derived factor-1 and its unique chemokine receptor) axis in LPS-induced bone loss has not been studied. The aim of this study was to investigate the role of the SDF-1/CXCR4 axis in LPS-stimulated inflammatory bone loss. The results show that LPS does not influence the expression of SDF-1/CXCR4 in osteoblasts, but up-regulates the expression of CXCR4 in pre-osteoclasts via Toll-like receptor 4, which subsequently enhances pre-osteoclast migration. Moreover, LPS promoted RANKL-induced osteoclast differentiation partially through CXCR4 up-regulation. In conclusion, the present study demonstrated, for the first time, that the up-regulated expression of CXCR4 in pre-osteoclasts by LPS stimulation is involved in LPS-induced bone resorption.