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. 2018 Dec 14;8:17870. doi: 10.1038/s41598-018-35943-x

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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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Transcriptional and epigenetic analysis of Klotho (KI) gene in AKI and CKD models. RT-qPCR RNA and ChIP-qPCR analysis (see Fig. 4). Klotho transcript levels (mRNA) were normalized to L32 mRNA. Matrix ChIP-qPCR analysis RNA polymerase II (Pol II), and permissive (H3K27Ac, H3K4m3) and repressive (H3K9m2) marks (n = 6 mice from each group). Small solid circle, p < 0.05, large circle, p < 0.01, and no circle, not statistically significant. The downregulated Klotho transcripts were not matched by Pol II levels suggesting that post-transcriptional mechanisms are playing a role (e.g. splicing, message stability). Here, the epigenetic changes that correspond to mRNA levels could be playing a role.