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. 2018 Jan 24;8:1510. doi: 10.1038/s41598-018-20027-7

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© The Author(s) 2018

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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Barrier function assay in mouse and human endothelial cells. Electric cell-substrate impedance sensing (ECIS) measurement of endothelial resistance. (A and C) Real time tracings (representative of 4 independent monolayers) in MECs and HUVECs starting at the time of addition of specific antibodies or isotype controls. Presented resistance is normalized to a pre-treatment time-point for comparison of mAb effect on barrier function. (B) Quantification of AUC normalized to no treatment control. Anti-PECAM-1 antibodies had no effects on the electrical resistance of MEC monolayers in comparison to no treatment or isotype control (^#p = 0.97, 0.99 for solo mAbs and 0.51 for a combination, respectively). Data shown as mean ± SD, dotted line illustrating a level of no treatment control. (D) In quiescent HUVEC cells, binding to PECAM-1, both solo and paired, results in significant drop in endothelial resistance (*p < 0.01, compared to no treatment). Effect mAbs to PECAM-1, when compared to IgG isotype control, was not significant (^#p = 0.36 for Ab62 vs. mouse IgG2A and p = 0.81, for Ab37 vs. mouse IgG1). In both systems, significant barrier disruption was seen after binding of mAb to VE-cadherin (**p = 0.0005; ***p < 0.0001, compared to IgG isotype control). Data shown as mean ± SD, dotted line illustrating a level of no treatment control.