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. 2017 Aug 15;7:8296. doi: 10.1038/s41598-017-08373-4

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© The Author(s) 2017

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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Endothelial-targeted antioxidant enzymes reverse increased micro-vessel permeability in KRIT1 deficient mice. (A) Cremaster arteriole permeability in KRIT1 heterozygous (Krit1^+/−) mice treated with PECAM-AOE, unconjugated AOE, or vehicle alone +/− TNF-α. n = 10 vessel sites; p < 0.001 by non-parametric ANOVA; *p < 0.05 by Dunn’s post-hoc test, n.s.- not significant. (B) Cremaster venule permeability under same conditions as in (A). p < 0.001 by non-parametric ANOVA; *p < 0.05 by Dunn’s post-hoc test, n.s.- not significant. (C) Cremaster arteriole permeability in wild type (Krit1^+/+) mice treated with PECAM-AOE, unconjugated AOE, or vehicle alone in the presence or absence of TNF-α. Data shown are the mean P_s +/− SEM. n = 10 vessel sites; p < 0.001 by non-parametric ANOVA; *p < 0.05 by Dunn’s post-hoc testing.(D) Cremaster venule permeability under same conditions as in (A). p < 0.001 by non-parametric ANOVA; *p < 0.01 or ^#p < 0.05 by Dunn’s post-hoc test, n.s.- not significant.