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. 2018 May 15;8:7569. doi: 10.1038/s41598-018-25853-3

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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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Schematic demonstration of TNT formation. WGA acts on sialic acid residues exposed on the extracellular surface of CD31 transducing signals to actin binding proteins and triggering changes in actin distribution. Thrombin acts via its PAR1 receptor initiating an intracellular signalling cascade involving PKCα and impacts upon actin binding proteins. TNTs are formed in endothelial cells as cells move apart.