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. 2020 Jun 18;10:9926. doi: 10.1038/s41598-020-66568-8

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© The Author(s) 2020

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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Hypoxia prevents loss of endothelial barrier function and VE-cadherin disruption mediated by CA4P. (a) Endothelial cells cultured to confluence in 3 μm pore size filter inserts set in companion 24-well plates were exposed to the indicated oxygen levels for 14 h and then to CA4P (1 μM) for an further 15 min. FITC dextran diffusion through the monolayers during 30 min, was expressed as fold change over control untreated cells maintained in 21% O_2.. Results are from 5–7 independent experiments. Data were analysed by one-way Anova followed by a Tukey post-test. Values are means ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). (b) Cells in 21% or 0.1% O₂ for 14 h were treated with CA4P as in (a) and then fixed and stained for VE-cadherin.