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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.

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Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Department of Radiology, Zhongshan Hospital and Shanghai Institute of Medical Imaging, Department of Medical Imaging, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Nanjing University of Traditional Chinese Medicine Hanlin College Affiliated Hai'an Chinese Medicine Hospital, Nanjing University of Traditional Chinese Medicine, Haian, Jiangsu, China.
Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Department of Pathogen Biology, Medical College, Nantong University, Nantong, 2266001, Jiangsu, China.


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.


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

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