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蛋白质组学鉴定神经性疼痛模型大鼠脊髓中上调的膜联蛋白A3同种型

Proteomic Identification of an Upregulated Isoform of Annexin A3 in the Spinal Cords of Rats in a Neuropathic Pain Model.

作者信息

Zou Wangyuan, Xu Wei, Song Zongbin, Zhong Tao, Weng Yingqi, Huang Changsheng, Li Maoyu, Zhang Chuanlei, Zhan Xianquan, Guo Qulian

机构信息

Department of Anesthesiology, Xiangya Hospital, Central South UniversityChangsha, China.

Key Laboratory of Cancer Proteomics of Chinese Ministry of Health, Xiangya Hospital, Central South UniversityChangsha, China.

出版信息

Front Neurosci. 2017 Sep 5;11:484. doi: 10.3389/fnins.2017.00484. eCollection 2017.

DOI:10.3389/fnins.2017.00484
PMID:28928629
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5591859/
Abstract

Neuropathic pain (NP) is induced by nerve damage or a disturbance in the peripheral or central nervous systems. Nerve damage causes the activation of sensitizing mechanisms in the peripheral and central nervous systems, which induces transcriptional and post-transcriptional alterations in sensory nerves. However, the underlying mechanisms of NP remain elusive. In the study, Two-dimensional gel electrophoresis (2DGE)-based comparative proteomics identified 38 differential gel spots, and 15 differentially expressed proteins (DEPs) between the sham and the chronic constriction injury (CCI)-induced neuropathic pain rats. Of them, Annexin A3 (ANXA3) was significantly increased after CCI with Western blot analysis and immunofluorescence imaging. A lentivirus delivering ANXA3 shRNA (LV-shANXA3) was administered intrathecally to determine the analgesic effects of ANXA3 on allodynia and hyperalgesia in a CCI-induced neuropathic pain model in rats. Further study showed that LV-shANXA3 reversed the upregulation of ANXA3, alleviated CCI-induced mechanical allodynia and thermal hyperalgesia. The study indicated that ANXA3 may play an important role in neuropathic pain.

摘要

神经性疼痛(NP)由神经损伤或外周或中枢神经系统紊乱引起。神经损伤会导致外周和中枢神经系统中的敏化机制激活,进而引起感觉神经的转录和转录后改变。然而,NP的潜在机制仍不清楚。在该研究中,基于二维凝胶电泳(2DGE)的比较蛋白质组学在假手术组和慢性压迫性损伤(CCI)诱导的神经性疼痛大鼠之间鉴定出38个差异凝胶点和15种差异表达蛋白(DEP)。其中,通过蛋白质免疫印迹分析和免疫荧光成像发现,CCI后膜联蛋白A3(ANXA3)显著增加。将携带ANXA3短发夹RNA(LV-shANXA3)的慢病毒鞘内注射,以确定ANXA3对CCI诱导的大鼠神经性疼痛模型中异常性疼痛和痛觉过敏的镇痛作用。进一步研究表明,LV-shANXA3可逆转ANXA3的上调,减轻CCI诱导的机械性异常性疼痛和热痛觉过敏。该研究表明,ANXA3可能在神经性疼痛中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33dd/5591859/93382bc8464b/fnins-11-00484-g0007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33dd/5591859/24db6d3f79e7/fnins-11-00484-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33dd/5591859/1e025bba1225/fnins-11-00484-g0002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33dd/5591859/482d53510757/fnins-11-00484-g0005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33dd/5591859/93382bc8464b/fnins-11-00484-g0007.jpg

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