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. 2019 Sep 3;116(8):1525–1538. doi: 10.1093/cvr/cvz238

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© The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Schematic diagram summarizing the effects of inflammation induced EC-MVs on endothelial and neutrophil activation. Inflammatory injury increases the production of endothelial microvesicles. Src⁺ EC-MVs disrupt endothelial barrier integrity by increasing acto-myosin contractility through stress fibre formation and increased phosphorylation of MLCK. Src⁺ EC-MVs increase tyrosine phosphorylation of VE-cadherin and increase albumin permeability through endothelial monolayers. EC-MVs also contribute to vascular injury indirectly by increasing adhesion molecules on ECs and neutrophils to enhance PMN-EC adhesion and by promoting NETosis with release of citrullinated histone H3 and myeloperoxidase. Images of cells were obtained from Smart Servier Medical Art (https://smart.servier.com).