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. 2021 Jan 18;28(6):1865–1879. doi: 10.1038/s41418-020-00713-8

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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 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 LC3 puncta were increased in ETO-treated RPE1 cells as shown by immunostaining with an antibody against LC3. DNA was stained with DAPI (blue). Scale bar, 10 µm. B Quantitative results of LC3 puncta per cell of RPE1 cells upon ETO treatment for 24 h. Increased LC3 II to I ratio in ETO-treated RPE1 cells. C Extracts of ETO-treated RPE1 cells were analyzed by immunoblotting with antibodies against LC3 and actin. Quantitative results of relative intensity of LC3 II/ I (D) and LC3 II/actin (E) of C. ETO-treated data were normalized to the data without ETO treatment. Reduced p62 abundance in ETO-treated RPE1 cells. F Extracts of ETO-treated RPE1 cells were analyzed by immunoblotting with antibodies against p62 and actin. G Quantitative results of relative intensity of p62 of F. **P < 0.01; ***P < 0.001; n.s. no significance.