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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. 6 — The anti-inflammatory effect of hCSSC on mouse stromal wound model was attenuated by TGFβ3 knockdown. After cell treatment for 1 day, mouse specific early inflammatory genes (CD80, CXCL5, Lcn2, PLAUR, Ppbp and Spp1) were upregulated in the wounded corneas, as compared to naïve corneas. Gene expression was suppressed by hCSSC treatment, representing an anti-inflammatory effect. Such a response was attenuated when hCSSC-TGFβ3(si) were applied. Mean and SD represent data from triplicate experiments. *P < 0.05, paired Student’s t-test