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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. 2 — Silencing of PTP4A1 downregulates pro-fibrotic genes in NHDF. a Agarose gel with RT-PCR of PTP4A1 mRNA from NHDF lines treated with control ASO (left lane) or with PTP4A1 ASO (right lane). b The heat map shows gene expression levels of three different NHDF lines (L1–3) treated with control ASO or PTP4A1 ASO. NGS was performed in triplicate for each NHDF line. c List of human pro-fibrotic genes downregulated in PTP4A1 KD NHDF lines, after DESeq analysis. d, e Left graphs show mean ± SEM of SMAD3 and ACTA2 mRNA expression measured in six different NHDF lines treated with PTP4A1 ASO and normalized to same lines treated with control ASO. Right graphs show mean ± SEM of densitometric scan expression plus representative immunoblotting for SMAD3 and αSMA (upper bands) normalized to GAPDH (lower bands) in six different NHDF lines treated with control ASO or PTP4A1 ASO. Wilcoxon test (d, e left) or Mann–Whitney test (d, e right)