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. 2018 Sep 5;8:13229. doi: 10.1038/s41598-018-31408-3

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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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Mechanisms of histamine-induced endothelial barrier disruption. Under resting conditions, vinculin is localized mainly along endothelial cell borders and at least in part co-localizes with VE-cadherin and α-catenin at AJs. In anaphylaxis, histamine induces a rapid increase of cytoplasmic Ca²⁺ leading to activation of RhoA. Both events induce stress fiber formation at focal adhesions. In addition, RhoA via Rho kinase may enhance tension on α-catenin at endothelial AJs which causes AJ reorganization. H1R = Histamine receptor type I; Ca²⁺ = calcium; MLC = myosin light chain; FAK = focal adhesion kinase; VASP = vasodilator-stimulated phosphoprotein; ZO-1 = zonula occludens protein1; α, β, γ = α-, β-, γ-catenin; ECM = extracellular matrix.