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