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Fascin-1 Contributes to Neuropathic Pain by Promoting Inflammation in Rat Spinal Cord.

Authors
  • Wang, Binbin1
  • Fan, Bingbing2
  • Dai, Qijun3
  • Xu, Xingguo1
  • Jiang, Peipei3
  • Zhu, Lin3
  • Dai, Haifeng3
  • Yao, Zhigang3
  • Xu, Zhongling4
  • Liu, Xiaojuan5
  • 1 Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China. , (China)
  • 2 Department of Radiology, Zhongshan Hospital and Shanghai Institute of Medical Imaging, Department of Medical Imaging, Shanghai Medical College, Fudan University, Shanghai, 200032, China. , (China)
  • 3 Nanjing University of Traditional Chinese Medicine Hanlin College Affiliated Hai'an Chinese Medicine Hospital, Nanjing University of Traditional Chinese Medicine, Haian, Jiangsu, China. , (China)
  • 4 Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China. [email protected] , (China)
  • 5 Department of Pathogen Biology, Medical College, Nantong University, Nantong, 2266001, Jiangsu, China. [email protected] , (China)
Type
Published Article
Journal
Neurochemical Research
Publisher
Springer-Verlag
Publication Date
Feb 01, 2018
Volume
43
Issue
2
Pages
287–296
Identifiers
DOI: 10.1007/s11064-017-2420-8
PMID: 29052088
Source
Medline
Keywords
License
Unknown

Abstract

Neuropathic pain is a complicated clinical syndrome caused by heterogeneous etiology. Despite the fact that the underlying mechanisms remain elusive, it is well accepted that neuroinflammation plays a critical role in the development of neuropathic pain. Fascin-1, an actin-bundling protein, has been proved to be involved in the processing of diverse biological events including cellular development, immunity, and tumor invasion etc. Recent studies have shown that Fascin-1 participates in antigen presentation and the regulation of pro-inflammatory agents. However, whether Fascin-1 is involved in neuropathic pain has not been reported. In the present study we examined the potential role of Fascin-1 by using a rodent model of chronic constriction injury (CCI). Our results showed that Fascin-1 increased rapidly in dorsal root ganglions (DRG) and spinal cord (SC) after CCI. The increased Fascin-1 widely expressed in DRG, however, it localized predominantly in microglia, seldom in neuron, and hardly in astrocyte in the SC. Intrathecal injection of Fascin-1 siRNA not only suppressed the activation of microglia and the release of pro-inflammatory mediators, but also attenuated the mechanical allodynia and thermal hyperalgesia induced by CCI.

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