| Literature DB >> 29736614 |
Dan-Ni Shi1, Yi-Tao Yuan1,2, Dan Ye3, Lu-Mei Kang4, Jing Wen1, Hong-Ping Chen5,6.
Abstract
MicroRNAs have been implicated in nerve injury and neuropathic pain. In the previous study we had shown that miR-96 can attenuate neuropathic pain through inhibition of Nav1.3. In this study, we investigated the role of miR-183, a same cluster member of microRNA with miR-96, in neuropathic pain and its potential mechanisms. We found that the expression level of miR-183-5p in dorsal root ganglion was decreased with the development of neuropathic pain induced by chronic constriction sciatic nerve injury (CCI). By contrast, the TREK-1, a K+ channel, was increased. Further investigation identified that intrathecal injection of miR-183-5p mimic efficiently ameliorated neuropathic pain and inhibited the expression of TREK-1, a predicted target gene of miR-183-5p. Luciferase assays confirmed the binding of miR-183-5p and TREK-1. In addition, over-expression of TREK-1 blocked the roles of miR-183-5p in neuropathic pain. Our findings suggested that miR-183-5P participated in the regulation of CCI-induced neuropathic pain through inhibiting the expression of TREK-1.Entities:
Keywords: Chronic constriction injury; Dorsal root ganglion; MiR-183-5p; Neuropathic pain; TREK-1
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Year: 2018 PMID: 29736614 DOI: 10.1007/s11064-018-2529-4
Source DB: PubMed Journal: Neurochem Res ISSN: 0364-3190 Impact factor: 3.996