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Neurochem Res. 2018 Feb;43(2):287-296. doi: 10.1007/s11064-017-2420-8. Epub 2017 Oct 19.

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

Author information

1
Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, 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.
3
Nanjing University of Traditional Chinese Medicine Hanlin College Affiliated Hai'an Chinese Medicine Hospital, Nanjing University of Traditional Chinese Medicine, Haian, Jiangsu, China.
4
Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China. jsrdwbb1@sohu.com.
5
Department of Pathogen Biology, Medical College, Nantong University, Nantong, 2266001, Jiangsu, China. lxj@ntu.edu.cn.

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.

KEYWORDS:

Fascin-1; IL-6; Inflammation; Microglia; Neuropathic pain; TNF-α

PMID:
29052088
DOI:
10.1007/s11064-017-2420-8
[Indexed for MEDLINE]

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