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. 2019 Feb 13;9:1920. doi: 10.1038/s41598-019-38566-y

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© The Author(s) 2019

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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Anti-miR-17 treatment reduced fibrosis, inflammation, and M2-like macrophages. (A,B) Q-PCR analysis demonstrated that the expression of fibrosis and inflammation-related genes is markedly increased in PBS-treated Pkd1-KO kidneys compared to control (non-cystic) kidneys. Expression of these genes was reduced in anti-miR-17-treated kidneys compared to PBS-treated kidneys. Anti-miR-18 treatment did not affect the expression of fibrosis-related genes but reduced the expression many inflammation-related genes (N = 5 per group). (C) Q-PCR analysis of M2-like macrophage markers Arg1 and Mrc1 in the indicated groups is shown. (D) Western blot and immunofluorescence analysis revealed that MRC1 expression was increased in PBS-treated Pkd1-KO compared to control (non-cystic) kidneys. Both anti-miR-17 and anti-miR-18 treatment reduced MRC1 expression. Data are presented as mean ± SEM. Statistical analyses: Student’s t-test, ns indicates P > 0.05.