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. 2017 Nov 1;7:14811. doi: 10.1038/s41598-017-13694-5

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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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P38 and ERK signaling pathways are critical to cadmium-induced tube formation dysfunction in H9-ECs. (A) Representative confocal images showing the rescuing effect of CdCl₂-induced tube formation dysfunction phenotype in H9-ECs by a panel of inhibitors to block ERK, P38, Wnt and ErbB, respectively. (B–C) Bar graphs to compare the number of tube-like structures and tube length between different groups in (A). ^*** P < 0.001, ^**** P < 0.0001, when compared to control cells; ^# P < 0.05, ^## P < 0.01, ^### P < 0.001, ^#### P < 0.0001, when compared to CdCl₂-treated cells.