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. 2020 May 7;11(5):327. doi: 10.1038/s41419-020-2510-4

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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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Fig. 5 — a Expression of CK1δ and β-TRCP in hucMSC-Ex was determined by western blot and qRT-PCR. b Representative images of HE and Masson staining in the UUO model with hucMSC-Ex, shCK1δ-Ex, and shβ-TRCP-Ex. Bar = 100 μm. c Double immunofluorescent staining of YAP and α-SMA in the kidneys of the UUO model treated with hucMSC-Ex, shCK1δ-Ex, and shβ-TRCP-Ex. Bar = 50 μm. d Western blot analyses for CK1δ and β-TRCP in NRK-52E after hucMSC-Ex treatment. e The expression of CK1δ, β-TRCP, YAP, and α-SMA in UUO14d with hucMSC-Ex, shCK1δ-Ex, and shβ-TRCP-Ex treatment was detected by western blot. f A proposed hypothesis for hucMSC-Ex attenuated tubulointerstitial fibrosis through CK1δ and β-TRCP mediated YAP ubiquitination and degradation.