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. 2020 Jul 2;12:98. doi: 10.1186/s13148-020-00892-8

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — Tet2 deficiency boosts inflammation in the kidney upon IR injury. The IR-insulted kidney tissues from WT and Tet2^−/− mice (n = 3 in each genotype) were subjected to RNA-seq analysis. a Scatter plotting of the differentially expressed genes in the IR-insulted kidney tissues from WT and Tet2^−/− mice. Green dot, downregulated genes; red dot, upregulated genes. b Top 10 terms of the pathway analysis of the upregulated DEGs in the IR-insulted kidney between WT and Tet2^−/− mice. c Heatmap showing the augmented expression of renal inflammation-related genes. d, e The mRNA levels of IL6 (d) and TNF-alpha (e) were measured by qRT-PCR. *P < 0.05 and **P < 0.01. N = 3 in each group. f Top 10 terms in the pathway analysis of downregulated DEGs in the IR-insulted kidney between WT and Tet2^−/− mice