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MiR-183-5p Alleviates Chronic Constriction Injury-Induced Neuropathic Pain Through Inhibition of TREK-1

机译:MiR-183-5P通过抑制Trek-1减轻慢性收缩损伤诱发的神经性疼痛

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摘要

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.
机译:MicroRNA涉及神经损伤和神经性疼痛。在以前的研究中,我们表明MIR-96可以通过NAV1.3的抑制来衰减神经性疼痛。在这项研究中,我们调查了MiR-183,MicroRNA与miR-96的相同簇成员在神经性疼痛及其潜在机制中的作用。我们发现,随着慢性限制坐骨神经损伤(CCI)诱导的神经性疼痛的发育,下降型背根神经节的miR-183-5p的表达水平降低。相反,Trek-1,K +通道增加。进一步调查鉴定出MiR-183-5P的鞘内注射有效地改善神经性疼痛,并抑制Trek-1的表达,预测miR-183-5p的靶基因。荧光素酶测定证实了miR-183-5p和trek-1的结合。此外,Trek-1的过表达阻断了miR-183-5p在神经性疼痛中的作用。我们的研究结果表明,MIR-183-5P通过抑制Trek-1的表达,参与CCI诱导的神经性疼痛的调节。

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