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. 2021 Oct 4;57(8):763–774. doi: 10.1007/s11626-021-00606-1

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© The Author(s) 2021

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. 3. — The Egr1 3′ UTR was regulated by miR-23a-3p. (A, B) miR-23a-3p expression was measured by qRT-PCR in DKD mice and BSA-induced HK-2 cells. (C) The efficiency of the miR-23a-3p mimic was determined by qRT-PCR. (D–F) The mRNA and protein expression levels of Egr1 were detected in BSA-induced HK-2 cells transfected with the miR-23a-3p mimic for 48 h. (G) The efficiency of the miR-23a-3p inhibitor was determined by qRT-PCR. (H–J) The mRNA and protein expression levels of Egr1 were detected in BSA-induced HK-2 cells transfected with the miR-23a-3p inhibitor for 48 h. (K) Putative binding sequence of miR-23a-3p in the 3′ UTR of Egr1. The putative binding sequence was eliminated in mutant-type Egr1 3′ UTR luciferase reporter plasmids. (L) Luciferase assays of 293T cells cotransfected with the miR-23a-3p mimic combined with wild- or mutant-type Egr1 3′ UTR luciferase reporter plasmids. Student’s t-test was used to analyze the statistical significance. Data are reported as the mean ± SEM. *P < 0.05 and **P < 0.01.