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. 2020 Aug 12;11:348. doi: 10.1186/s13287-020-01829-x

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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. 2 — Overexpression of miR-203 reduce the number of ESCs and impaired their proliferation capacity. K15+ and P63+ cell in normal rats and rats with type 2 diabetes wounded skin (a). mRNA expression of K15, P63, and Intergrin-β1 in normal rats and rats with type 2 diabetes wounded skin (b). Colony-forming assay for mannitol/glucose-incubated ESCs (c, d). Overexpression of miR-203reduce expression of K15, K19, P63, and Intergrin-β1 (e). Inhibition of miR-203 improve colony-forming assay for mannitol/glucose-incubated ESCs (f, g). Data are representative profile of clustered miRNA in individual samples and expressed as the mean ± SD of each group of samples from at least three separate experiments. *p < 0.05; **p < 0.01; ***p < 0.001