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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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Effect of PRX on mouse cerebral endothelial cell permeability. L-PRX was expressed in primary mouse cerebral endothelial cells using recombinant lentiviruses. Uninfected cells were used as a control. At the number of days after infection indicated on the x-axis, permeability to indicated fluorescent tracers was determined (A–C). (D) TEER was also determined at the same time points. L-PRX significantly strengthened the barrier function of endothelial cells, accelerating both the acquisition of barrier function and the final resistance of cells to tracers of a wide range of molecules. RFP lentivirus infected cells showed the same permeability profiles as uninfected cells (not shown). Data represent means +/− SD for n = 5 independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 comparing control and L-PRX transfected cells.