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. 2020 Nov 16;473(1):79–93. doi: 10.1007/s00424-020-02491-1

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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 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/.

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Fig. 4 — DCT cell proliferation rate in Prox-1_DCT^Ctrl versus Prox-1_DCT^KO mice in response to a 3-day treatment with bumetanide. A Paraffin sections of Prox-1_DCT^Ctrl mice kidneys (upper panel) and Prox-1_DCT^KO mice kidneys (lower panel) after a 3-day treatment with bumetanide and BrdU (right) or BrdU only (left). A double-immunostaining for NCC (red) and BrdU (green) allowed for the identification of DCT segments and proliferating DCT cells. B A significant increase in DCT cell proliferation rate was achieved in Prox-1_DCT^Ctrl (p = 0.0001) and Prox-1_DCT^KO (p = 0.0007) by the administration of bumetanide and BrdU compared to the situation where mice received BrdU only. However, no difference in the proliferation rate between the different genotypes was observed. Data are mean ± SEM, n = 6 (BrdU only), n = 5 (Bumetanide + BrdU, ctrl), n = 4 (Bumetanide + BrdU, ko)