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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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Mapping structural domains of PRX that mediate enhancement of endothelial permeability. The effect of three components of PRX on endothelial permeability was compared. Lentiviruses were used to express either full length L-PRX, S-PRX, or D-PRX (C-terminal PRX) (similar to the sequences shown in Fig. 4A, minus the GFP tag) and permeability was measured as in Fig. 6 for each group of infected primary mouse brain endothelial cells. Permeability to both inulin (A) and dextran (B) were measured. Enhancement of barrier function was observed in cells expressing S-PRX and full length L-PRX, but not with D-PRX. 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 < 0.05, **p < 0.01, ***p < 0.001, comparing control and S-, D- and L-PRX transfected cells. ^###p < 0.001 comparing L-PRX with S- and D-PRX transfected cells.