MicroRNA-182 Alleviates Neuropathic Pain by Regulating Nav1.7 Following Spared Nerve Injury in Rats.

MicroRNA-182 Alleviates Neuropathic Pain by Regulating Nav1.7 Following Spared Nerve Injury in Rats.
复制标题

MicroRNA-182 通过调节大鼠神经损伤后的 Nav1.7 减轻神经性疼痛

DOI:
10.1038/s41598-018-34755-3
复制
发表时间:
2018-11-13
期刊:
影响因子:
4.6
通讯作者:
Zang W
Zang W
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Cai W;Zhao Q;Shao J;Zhang J;Li L;Ren X;Su S;Bai Q;Li M;Chen X;Wang J;Cao J;Zang W

文献摘要

参考文献

被引文献

相似文献

钠通道1.7(Nav1.7)由SCN9A基因编码,与神经病理性疼痛有关。作为基因表达的关键调节因子,许多miRNAs已经在神经病理性疼痛中发挥了重要作用,包括miR-182,它被预测为调节SCN9A基因。备用神经损伤(SNI)可上调L4-L6背根节(DRGs)Nav1.7的表达,而SNI后miR-182的表达下调。探索Nav1.7和miR-182之间的联系可能有助于开发更好的靶向治疗。在目前的研究中,miR-182与SCN9A基因的直接配对是通过体外荧光素酶试验来验证的。微量注射miR-182可逆转SNI大鼠L4-6背根节Nav1.7基因表达水平的异常升高,并显著减轻其对机械刺激的超敏反应。相反,给予miR-182 antagomir后,幼稚大鼠L4-6背根节Nav1.7基因的表达增强,并伴随着机械超敏反应的产生。总之,我们得出结论,miR-182可以通过调节Nav1.7来减轻SNI诱导的大鼠神经病理性疼痛。
The sodium channel 1.7 (Nav1.7), which is encoded by SCN9A gene, is involved in neuropathic pain. As crucial regulators of gene expression, many miRNAs have already gained importance in neuropathic pain, including miR-182, which is predicted to regulate the SCN9A gene. Nav1.7 expression in L4-L6 dorsal root ganglions (DRGs) can be up regulated by spared nerve injury (SNI), while miR-182 expression was down regulated following SNI model. Exploring the connection between Nav1.7 and miR-182 may facilitate the development of a better-targeted therapy. In the current study, direct pairing of miR-182 with the SCN9A gene was verified using a luciferase assay in vitro. Over-expression of miR-182 via microinjection of miR-182 agomir reversed the abnormal increase of Nav1.7 at both mRNA and protein level in L4-6 DRGs of SNI rats, and significantly attenuated the hypersensitivity to mechanical stimulus in the rats. In contrast, administration of miR-182 antagomir enhanced the Nav1.7 expression at both mRNA and protein level in L4-6 DRGs, companied with the generation of mechanical hypersensitivity in naïve rats. Collectively, we concluded that miR-182 can alleviate SNI- induced neuropathic pain through regulating Nav1.7 in rats.
DOI: 10.1016/j.bbi.2016.12.012
发表时间: 2017-03
期刊: Brain, behavior, and immunity
影响因子: --
作者:
Lan X;Han X;Li Q;Li Q;Gao Y;Cheng T;Wan J;Zhu W;Wang J
通讯作者: Wang J
DOI: 10.1016/j.expneurol.2016.06.025
发表时间: 2016-09
影响因子: 5.3
作者:
Leinders M;Üçeyler N;Pritchard RA;Sommer C;Sorkin LS
通讯作者: Sorkin LS
DOI: 10.1016/j.pain.2014.08.003
发表时间: 2014-10-01
期刊: PAIN
影响因子: 7.4
作者:
Harrer, Judith U.;Uceyler, Nurcan;Sommer, Claudia
通讯作者: Sommer, Claudia
DOI: 10.1146/annurev.neuro.051508.135531
发表时间: 2009
影响因子: 13.9
作者:
Costigan M;Scholz J;Woolf CJ
通讯作者: Woolf CJ
DOI: 10.1016/j.pain.2005.10.036
发表时间: 2006-05-01
期刊: PAIN
影响因子: 7.4
作者:
Bourquin, Anne-Frederique;Sueveges, Maria;Decosterd, Isabelle
通讯作者: Decosterd, Isabelle