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. 2018 Oct 29;8:15913. doi: 10.1038/s41598-018-34277-y

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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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Genomic organization, structure and expression of miR-183 and the miR-200 gene clusters involved in alcohol abuse and the TLR4 immune response. (A) Homology sequence with a conserved seed¹²¹ of the miR components of the mmu-miR-183 cluster (miRs-183, -96, -182) on assembly mouse (Chromosome (Chr.) 6, Chr.7 human homolog). (B) The miR-200 family forms two clusters located in different genomic regions: cluster I miR-200s (miR-200b, -200a, -429) and cluster II miR-200s (−200c, −141) located in assembly mouse (Chr. 4 and Chr. 6, respectively) and divided into two functional groups based on their seed sequences¹²¹. (C) NGS data show that ethanol treatment causes a statistical significant expression (fold change, statistic, p-value (pval), p-value adjusted (padj)) of the selected miRs (miR-96, -182, -183, -200a and -200b). (D) The RT-qPCR shows a differential expression at the levels of miR-183, miR-182, miR-96 (miR-183C), miR-200a and miR-200b in the cortices of the ethanol-treated vs. untreated WT and TLR4-KO mice. n = 9–11 independent experiments. *p < 0.05, **p < 0.01 (Student’s t-test).