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. 2021 May 25;13:116. doi: 10.1186/s13148-021-01103-8

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© The Author(s) 2021

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. 2 — In vitro decidualization and the regulation of epigenetic processes. On the left side of the figure are shown the different methodologies used to induce in vitro decidualization. On the right side of the figure are shown the effects of in vitro decidualization on the content of epigenetic processes and components. Estradiol and progesterone downregulate the expression of DNMT1 (mainly by progesterone) and DNMT3b (mainly by estradiol), increase the enrichment H3K27ac and H3K4me3 in the promoter regions of genes associated with insulin signaling, increase the global content of H3K27ac and H3K4me1, and decrease the global content of H3K4me3. Progesterone and cAMP increase the enrichment of H3K27me3 in the promoter region of WNT4, ZBTB16, PROK1, and GREB1 genes. Estradiol, progesterone, and cAMP downregulate the expression of DNMT3b and transiently decrease the expression of DNMT1 and DNMT3a