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. 2019 Jul 1;11(3):21. doi: 10.1038/s41368-019-0054-1

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© The Author(s) 2019

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. 10 — TNF-α induced EndMT by upregulating the expression of EndMT markers in HUVECs. a Exposure of HUVECs to TNF-α (10 ng/ml) for 2 days induced morphological changes (bright field) and increased the level of fibroblast-specific protein-1 (FSP-1) in HUVECs. Scale bars: 50 μm. b Expression levels of EndMT-related genes determined by qPCR. Beta-actin served as loading control. c Representative Western blots of EndMT-related signaling molecules as well as mesenchymal and endothelial proteins. *P < 0.05; **P < 0.01 in one-way ANOVA. Results represent the means ± SD performed in triplicate