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. 2019 Mar 14;9:4596. doi: 10.1038/s41598-019-40795-0

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© The Author(s) 2019

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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CUL3 expression is dysregulated in AKI/CKD mouse models and human kidney tissue. (a) Immunofluorescence of consecutive kidney sections from control mice 72 h after IRI revealed decreased signal for CUL3 in most KIM-1⁺ tubules. n = 3. (b) Immunohistochemistry revealed strong CUL3 signal in sham mice in contrast to tubule cells 14 days after IRI. n = 3. (c) 14 days after unilateral ureteral obstruction (UUO), tubules had lower CUL3 signal and were adjacent to areas of increased alpha smooth muscle actin (α-SMA)⁺ extracellular matrix accumulation. n = 3. (d) Similar to (c), 7 days after injection of nephrotoxic serum, tubules had lower CUL3 signal and were adjacent to α-SMA⁺ areas. n = 3. (e) Human kidney tissue was obtained from tumour nephrectomy specimens and Periodic acid-Schiff stained sections of non-tumour renal tissue were assigned to the low-grade versus high-grade fibrosis groups. Immunohistochemistry revealed reduced CUL3 signal in high-grade fibrosis compared to low-grade fibrosis group. n = 3. Scale bars = 100 μm.