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. 2017 Jul 25;7:6349. doi: 10.1038/s41598-017-06484-6

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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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TLR4 deficiency protects the kidney from Ang-II mediated injury. (A) Representative images show Kidney injury molecule-1 immunofluorescence. Kidney sections from mice with normal TLR4 show increased KIM-1 fluorescence to Ang-II treatment in tubular areas (yellow arrows) compared to TLR4 deficiency mice (red arrow). (B) Data shows mean fluorescent intensity ± SEM. n = 5/group, tested by Kruskal-Wallis test. Scale bar - 50 µm. Magnification ×20. *p < 0.05 vs. C3HeJ + saline, ^†p < 0.05 vs. C3HeOuJ + Ang-II, ^‡p < 0.05 vs. C3HeOuJ + saline. C3HeOuJ: normal TLR4, C3HeJ: TLR4 deficiency.