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. 2019 Jun 19;9:8751. doi: 10.1038/s41598-019-45347-0

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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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Activation of EGFR and Stat3 in UUO-induced PrdxV^si kidney. To further verify the involvement of the EGFR and Stat3 signaling pathway in renal fibrosis aggravated by knockdown of PrdxV, the expression levels and activation levels of Stat3 and EGFR as an upstream molecule of Stat3 activation were assessed by western blotting. (a,b) Stat3 activation. Stat3 activation was analyzed by measuring phosphorylation at Tyr705 in Stat3. (c–f) Site-specific EGFR phosphorylation. The phosphorylation of EGFR at Tyr1068 was assessed with a specific anti-pEGFR Tyr1068 antibody. The phosphorylation levels of EGFR at Tyr1173 and Tyr845 were also checked as negative controls. Bar graphs show the mean ratios of the phosphorylated forms to the total level of the indicated targets as measured by densitometry. GAPDH was used as an internal control. All values are presented as mean ± SD. Statistical significance was measured using the one-way ANOVA with the Fisher least significant difference post-test. ^§p < 0.05; PrdxV^wt vs. PrdxV^si in UUO group.