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. 2020 Jan 15;10:386. doi: 10.1038/s41598-019-57286-x

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© The Author(s) 2020

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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PC2 levels are increased in pathologically stressed kidneys. (A) Normal (Sham) and AKI-afflicted mouse kidneys were immunoblotted for 4-HNE and PC2. Each band represents one biological replicate. Full-length blots shown in Fig. S6. (B,C) Quantification of 4-HNE and PC2 protein abundance in Sham and AKI kidneys, normalized to actin. *p < 0.05 as determined by Mann Whitney U test. Data presented as median with range. Sample size n = 3 biological replicates per group. (D) Normalized mRNA expression of Pkd2 in Sham and AKI-afflicted mouse kidneys. Gapdh used as internal control. Sample size n = 8 biological replicates per group. ***p < 0.001 as determined by Mann Whitney U test. Data presented as median with range. (E) Normal human kidneys (NHK) or kidneys with acute kidney injury (AKI) were stained for PC2 (green), DBA (red), a marker for collecting ducts, and VDAC (blue), an outer mitochondrial membrane protein. Scale bar, 75 μm.