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学科主题: 基础医学
题名:
EphrinB-EphB receptor signaling contributes to bone cancer pain via Toll-like receptor and proinflammatory cytokines in rat spinal cord
作者: Liu, Su1,2,3; Liu, Yue-Peng1,2,3; Song, William B.3; Song, Xue-Jun1,2,3
关键词: Bone cancer ; EphB1 ; TLR4 ; IL-1 beta ; TNF-alpha
刊名: PAIN
发表日期: 2013-12-01
DOI: 10.1016/j.pain.2013.08.017
卷: 154, 期:12, 页:2823-2835
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Anesthesiology ; Clinical Neurology ; Neurosciences
研究领域[WOS]: Anesthesiology ; Neurosciences & Neurology
关键词[WOS]: PERIPHERAL-NERVE INJURY ; NEURAL CREST MIGRATION ; PHYSICAL-DEPENDENCE ; NEUROPATHIC PAIN ; MICROGLIAL ACTIVATION ; GENE-EXPRESSION ; CELL INVASION ; UP-REGULATION ; GLIAL-CELLS ; MODEL
英文摘要:

Treating bone cancer pain poses a major clinical challenge, and the mechanisms underlying bone cancer pain remain elusive. EphrinB-EphB receptor signaling may contribute to bone cancer pain through N-methyl-D-aspartate receptor neuronal mechanisms. Here, we report that ephrinB-EphB signaling may also act through a Toll-like receptor 4 (TLR4)-glial cell mechanism in the spinal cord. Bone cancer pain was induced by tibia bone cavity tumor cell implantation (TCI) in rats. TCI increased the expression of TLR4 and the EphB1 receptor, the activation of astrocytes and microglial cells, and increased levels of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha). The increased expression of TLR4 and EphB1 were colocalized with each other in astrocytes and microglial cells. Spinal knockdown of TLR4 suppressed TCI-induced behavioral signs of bone cancer pain. The TCI-induced activation of astrocytes and microglial cells, as well as the increased levels of IL-1 beta and TNF-alpha, were inhibited by intrathecal administration of TLR4-targeting siRNA2 and the EphB receptor antagonist EphB2-Fc, respectively. The administration of EphB2-Fc suppressed the TCI-induced increase of TLR4 expression but siRNA2 failed to affect TCI-induced EphB1 expression. Intrathecal administration of an exogenous EphB1 receptor activator, ephrinB2-Fc, increased the expression of TLR4 and the levels of IL-1 beta and TNF-alpha, activated astrocytes and microglial cells, and induced thermal hypersensitivity. These ephrinB2-Fc-induced alterations were suppressed by spinal knockdown of TLR4. This study suggests that TLR4 may be a potential target for preventing or reversing bone cancer pain and other similar painful processes mediated by ephrinB-EphB receptor signaling. (C) 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

语种: 英语
所属项目编号: NSFC81271241 ; NSFC8132 0108012 ; NSFC81000475 ; BMU20120310 ; PCCRF-BSR11 120607
项目资助者: National Natural Science Foundation of China ; Peking University, Beijing, China ; Parker Research Foundation, Dallas, Texas, the United States
WOS记录号: WOS:000327596200034
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/53143
Appears in Collections:基础医学院_神经生物学系_期刊论文

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作者单位: 1.Parker Univ, Dept Neurobiol, Res Inst, Dallas, TX 75229 USA
2.Peking Univ, Neurosci Res Inst, Beijing 100191, Peoples R China
3.Peking Univ, Ctr Pain Med, Beijing 100191, Peoples R China

Recommended Citation:
Liu, Su,Liu, Yue-Peng,Song, William B.,et al. EphrinB-EphB receptor signaling contributes to bone cancer pain via Toll-like receptor and proinflammatory cytokines in rat spinal cord[J]. PAIN,2013,154(12):2823-2835.
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