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. 2020 Nov 3;7:52. doi: 10.1186/s40662-020-00217-z

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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. 5 — TGFβ3 was upregulated after hCSSC treatment to injured mouse corneas. After stromal ablation wounding, hCSSC or hCSSC-TGFβ3(si), suspended in fibrin gel, were applied to the fresh wounds. At 2 different time points, a 1 day and b 3 days, the expression of hTGFβ3 was significantly induced in corneas treated with hCSSC but not with hCSSC-TGFβ3(si). On the other hand, the expression of hTGFβ1 was not altered at either time points. The ratio of hTGFβ3/β1 was maintained between day 1 and day 3 post-treatment. Mean and SD represent data from triplicate experiments. *P < 0.05, paired Student’s t-test