Intrathecal miR-96 inhibits nav1.3 expression and alleviates neuropathic pain in rat following chronic construction injury
文献类型： 外文期刊
作者： Chen, Hong-Ping 1 ; Zhou, Wei 2 ; Kang, Lu-Mei 3 ; Yan, Han 4 ; Zhang, Lei 1 ; Xu, Bao-Hua 3 ; Cai, Wei-Hua 2 ;
作者机构： 1.Nanchang Univ, Coll Med, Dept Histol & Embryol, Nanchang 330006, Peoples R China
2.Nanjing Med Univ, Affiliated Hosp 1, Dept Orthopaed, Nanjing 210029, Jiangsu, Peoples R China
3.Nanchang Univ, Coll Med, Dept Anim Sci, Nanchang 330006, Peoples R China
4.Jiangxi Acad Agr Sci, Inst Qual Safety & Stand Agr Prod Res, Nanchang 330200, Peoples R China
关键词： Chronic constriction injury;Dorsal root ganglion;MiR-96;Nav1.3;Neuropathic pain
期刊名称：NEUROCHEMICAL RESEARCH （ 影响因子：3.996； 五年影响因子：3.858 ）
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收录情况： SCI
摘要： MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression post-transcriptionally by binding to their cognate target mRNAs. Emerging evidence suggests that miRNAs are critical regulators of neuronal functions. The expression pattern of miRNAs in the peripheral nervous system after peripheral nerve injury suggest that miRNAs may have important and yet unknown roles in the mechanisms of pain. Thus, we examined the role of miR-96 in neuropathic pain using a rat model of the condition chronic constriction sciatic nerve injury (CCI). We found that miR-96 alleviated neuropathic pain. The level of miR-96 was decreased within the ipsilateral dorsal root ganglion (DRG) after peripheral nerve injury but the Nav1.3 level was increased. Specifically, Intrathecal administration of miR-96 suppressed the expression of Nav1.3 induced by CCI. Further examination revealed that miR-96 inhibited the Nav1.3 mRNA expression in the embryonic DRG neurons in vitro. Our findings suggest that miR-96 participate in the regulation of neuropathic pain through inhibiting the expression of Nav1.3 in the DRG of CCI rats.
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