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

Weihua Cai, Qingzan Zhao, Jinping Shao, Jingjing Zhang, Lei Li, Xiuhua Ren, Songxue Su, Qian Bai, Ming Li, Xuemei Chen, Jian Wang, Jing Cao, Weidong Zang

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Article number16750
JournalScientific reports
Volume8
Issue number1
DOIs
StatePublished - Dec 1 2018

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Neuralgia
MicroRNAs
Spinal Ganglia
Wounds and Injuries
Hypersensitivity
Genes
Messenger RNA
Sodium Channels
Microinjections
Regulator Genes
Luciferases
Proteins
Gene Expression
Therapeutics

ASJC Scopus subject areas

  • General

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MicroRNA-182 Alleviates Neuropathic Pain by Regulating Nav1.7 Following Spared Nerve Injury in Rats. / Cai, Weihua; Zhao, Qingzan; Shao, Jinping; Zhang, Jingjing; Li, Lei; Ren, Xiuhua; Su, Songxue; Bai, Qian; Li, Ming; Chen, Xuemei; Wang, Jian; Cao, Jing; Zang, Weidong.

In: Scientific reports, Vol. 8, No. 1, 16750, 01.12.2018.

Research output: Contribution to journalArticle

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 2018, 'MicroRNA-182 Alleviates Neuropathic Pain by Regulating Nav1.7 Following Spared Nerve Injury in Rats', Scientific reports, vol. 8, no. 1, 16750. https://doi.org/10.1038/s41598-018-34755-3
Cai, Weihua ; Zhao, Qingzan ; Shao, Jinping ; Zhang, Jingjing ; Li, Lei ; Ren, Xiuhua ; Su, Songxue ; Bai, Qian ; Li, Ming ; Chen, Xuemei ; Wang, Jian ; Cao, Jing ; Zang, Weidong. / MicroRNA-182 Alleviates Neuropathic Pain by Regulating Nav1.7 Following Spared Nerve Injury in Rats. In: Scientific reports. 2018 ; Vol. 8, No. 1.
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abstract = "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 na{\"i}ve rats. Collectively, we concluded that miR-182 can alleviate SNI- induced neuropathic pain through regulating Nav1.7 in rats.",
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