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学科主题: 基础医学
题名:
LIMK-Dependent Actin Polymerization in Primary Sensory Neurons Promotes the Development of Inflammatory Heat Hyperalgesia in Rats
作者: Li, Yi1,2; Hu, Fang1,2; Chen, Hai-Jing1,2; Du, Yi-Juan1,2; Xie, Zhi-Ying3; Zhang, Ying1,2; Wang, Jun4; Wang, Yun1,2,5
刊名: SCIENCE SIGNALING
发表日期: 2014-06-24
DOI: 10.1126/scisignal.2005353
卷: 7, 期:331
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Cell Biology
研究领域[WOS]: Biochemistry & Molecular Biology ; Cell Biology
关键词[WOS]: PROTEIN-KINASE-C ; ROOT GANGLION NEURONS ; COFILIN PHOSPHORYLATION ; CYTOSKELETAL DYNAMICS ; THERMAL HYPERALGESIA ; CAPSAICIN RECEPTOR ; CELL-MIGRATION ; STRESS FIBERS ; ACTIVATION ; TRPV1
英文摘要:

Changes in the actin cytoskeleton in neurons are associated with synaptic plasticity and may also be involved in mechanisms of nociception. We found that the LIM motif-containing protein kinases (LIMKs), which regulate actin dynamics, promoted the development of inflammatory hyperalgesia (excessive sensitivity to painful stimuli). Pain is sensed by the primary sensory neurons of dorsal root ganglion (DRG). In rats injected with complete Freund′s adjuvant (CFA), which induces inflammatory heat hyperalgesia, DRG neurons showed an increase in LIMK activity and in the phosphorylation and thus inhibition of the LIMK substrate cofilin, an actin-severing protein. Manipulations that reduced LIMK activity or abundance, prevented the phosphorylation of cofilin, or disrupted actin filaments in DRG neurons attenuated CFA-induced heat hyperalgesia. Inflammatory stimuli stimulated actin polymerization and enhanced the response of the cation channel TRPV1 (transient receptor potential V1) to capsaicin in DRG neurons, effects that were reversed by the knockdown of LIMK or preventing cofilin phosphorylation. Furthermore, inflammatory stimuli caused the serine phosphorylation of TRPV1, which was abolished by preventing cofilin phosphorylation in DRG neurons. We conclude that LIMK-dependent actin rearrangement in primary sensory neurons, leading to altered TRPV1 sensitivity, is involved in the development of inflammatory hyperalgesia.

语种: 英语
所属项目编号: 91332119 ; 81161120497 ; 30925015 ; 30830044 ; 31371143 ; 30900582 ; 81221002 ; 30800330 ; 2014CB542204 ; 7132130
项目资助者: National Natural Science Foundation of China ; Ministry of Science and Technology of China ; Beijing Natural Science Foundation ; open project of the Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences
WOS记录号: WOS:000338511100003
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/67065
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.Beijing Huijia Private Sch, Beijing 102200, Peoples R China
2.Peking Univ, Sch Basic Med Sci, Minist Educ & Hlth, Neurosci Res Inst, Beijing 100191, Peoples R China
3.Peking Univ, Sch Basic Med Sci, Minist Educ & Hlth, Dept Neurobiol,Key Lab Neurosci, Beijing 100191, Peoples R China
4.Peking Univ, Sch Basic Med Sci, Dept Anat & Histol, Beijing 100191, Peoples R China
5.Peking Univ, PKU IDG McGovern Inst Brain Res, Beijing 100871, Peoples R China

Recommended Citation:
Li, Yi,Hu, Fang,Chen, Hai-Jing,et al. LIMK-Dependent Actin Polymerization in Primary Sensory Neurons Promotes the Development of Inflammatory Heat Hyperalgesia in Rats[J]. SCIENCE SIGNALING,2014,7(331).
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