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. 2017 Oct 20;8:1060. doi: 10.1038/s41467-017-01168-1

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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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Fig. 4 — PTP4A1 silencing protects mice from dermal fibrosis. Masson’s trichrome-stained skin sections from bleomycin-treated mice. Images are representative of 16 WT, 16 PTP4A1 KO, and 14 PTP4A1 KO/PTP4A2 Het mice (a), or 5 COL1A1Cre⁻/PTP4A1^fl/fl and 9 COL1A1Cre⁺/PTP4A1^fl/fl tamoxifen-induced mice (e). Graphs show mean ± SEM dermal thickness (b, g, see yellow bars in a and e), skin collagen concentration (c, h), and ACTA2 mRNA relative expression (d, i). f PTP4A1 mRNA relative expression in whole skin (left graph) or in isolated mouse dermal fibroblasts (right graph) from two COL1A1Cre⁻/PTP4A1^fl/fl or three COL1A1Cre⁺/PTP4A1^fl/fl mice. Mann–Whitney test. Scale bar, 50 μm