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. 2018 Nov 13;8:16750. doi: 10.1038/s41598-018-34755-3

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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miR-182 directly targets SCN9A 3′UTR. (A) The binding site of miR-182 within SCN9A 3′-UTR. The seed sequence is stressed in bold. (B) Co-localization of miR-182 with Nav1.7 in rat L5 DRG. Scale bar: 100 μm. (C) miR-182 agomir dose-dependently decreased the relative activity in PC12 cells transfected with SCN9A3′-UTR. One-way ANOVA followed by Tukey’s Multiple Comparison Test. F_3,8 = 86.367, **P < 0.01 vs. NC. n = 3 for each treatment. (D) The relative activity of luciferase in PC12 cells with wild type and mutant SCN9A 3′UTR after transfected with miR-182 agomir or scramble. n = 3 for each treatment. F_4,10 = 37.508. **P < 0.01 vs. WT+ vehicle. (E) Levels of miR-182 in L4-6 DRGs at days shown after SNI or sham surgery in rats. F_3,8 = 74.885 in SNI group, F_3,8 = 0.123 in sham group. **P < 0.01 vs. the baseline. n = 6 for each treatment.