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. 2017 Dec 14;7:17595. doi: 10.1038/s41598-017-18034-1

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© The Author(s) 2017

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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DNA methylation portrait. (a) Hierarchical clustering analysis based on epigenome-wide DNA methylation shows that the WJ MSC isolated from non-obese (n = 7) and obese donors (n = 7) cluster separately. WJ SMC from each donor were analysed in triplicates. (b) Principal component analysis (PCA) demonstrated that the WJ MSC from non-obese and obese donors formed separate clusters. (c) Manhattan plot indicates that altered methylation state was spread across all chromosomes. (d) Graphic showing percentage of differentially methylated CpG sites between averages of non-obese (n = 7) and obese (n = 7) samples. (e) Comparative analyses of WJ MSC from each obese donor vs. an average from all non-obese donors. Statistically significant alteration of methylation state was seen in 1–5% of all CpG sites in 6 out of 7 donors, whereas 32% of CpG sites were different in the samples from obese donor #5.