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. 2020 May 25;18:79. doi: 10.1186/s12964-020-00558-1

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 8 — Cx43^+/− mice exhibit minimal disassembly of the adherens and tight junction complex. Quantification of immunohistochemical staining determined an increase in N-cadherin (a & c) and decrease in ZO-1 (b & d) expression in wildtype (WT) UUO compared to WT sham controls. In Cx43^+/− (UUO) mice, expression of both markers was partially restored to near basal levels. Furthermore, western blotting (e) of renal cortex determined changes in expression of E-cadherin (f), β-catenin (g) and Claudin-2 (h) in WT UUO mice compared to WT shams, congruent to those found in vitro when cells were treated with TGF-β1. As expected, these changes were partially negated in Cx43^+/− (UUO) mice. Results were from six separate experiments; with significance shown: *P < 0.05; **P < 0.01; ***P < 0.001