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. 2018 Jul 3;8:10042. doi: 10.1038/s41598-018-28190-7

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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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PRX as an attenuator of inflammatory elevation of endothelial permeability. Murine endothelial cells were infected with viruses to express L-PRX. Afterwards, cells were challenged with LPS (5 ug/ml), which stimulates endothelial permeability. Measurements of permeability to a series of tracer proteins shown and of TEER demonstrate that L-PRX reduces LPS-stimulated permeability to proteins of a range of molecular weights. Uninfected cells served as controls. RFP lentivirus infected cells showed the same permeability profiles as uninfected cells (not shown). Data represent means +/− SD for n = 3 independent experiments. **p < 0.01, ***p < 0.001, comparing LPS-challenged to control cells. ^###p < 0.001 comparing L-PRX expressing to control cells.