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. 2018 Feb 14;8:3025. doi: 10.1038/s41598-018-21276-2

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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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Altered outer and inner retinal barrier function in diabetic HFE KO mice. (A) Tight junction protein Zonula occludin-1 (ZO-1) immunofluorescence in retinal pigment epithelium (RPE) flat mounts prepared from non-diabetic control and 16-week post-diabetic HFE WT and KO mice. (B) Western blot analysis of ZO-1 expression in protein extracted from the RPE of non-diabetic and diabetic HFE WT and KO mice. β-actin was used as a loading control. Blots cropped from different parts of the same gel or from different gels are separated by white space. (C) FITC-Dextran (40-kD) trans epithelial permeability assay performed on confluent monolayers of primary RPE cells established from HFE WT and HFE KO mouse eyes grown in normal glucose (5.5 mM) or high glucose (25 mM). Data are presented as mean ± S.E. *p < 0.01. (D) Fluorescein angiography and fundoscopic imaging of non-diabetic control vs diabetic HFE WT and KO mice.