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. 2022 Jul 29;13(7):662. doi: 10.1038/s41419-022-05121-z

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© The Author(s) 2022

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. 3 — A–D GPX1, GPX4, SOD1, SOD2 transcript levels were determined by qRT-PCR in DMOG and/or SI treated ARPE-19 cells. While GPX1 and GPX4 expression levels were mainly decreased by the treatments, especially SOD2 expression was upregulated by DMOG and DMOG + SI co-treatment compared to controls. E–H To validate if transcript levels reflected protein levels, GPX1, GPX4, and SOD2 protein levels were analyzed by Western blot. Only SOD2 protein levels were significantly increased by DMOG + SI co-treatment, which was also reflected by higher SOD activities (I, J). K In contradiction to the protective effect of SODs, SOD2 knockdown (SOD2 KD) rescued cells from cell death suggesting that SOD activity contributes to DMOG + SI-induced cells death. Data are presented as means + SD. Western blots (3-4 independent groups) and qRT-PCR (6 independent groups) were statistically analyzed with one-way ANOVA. SOD2 knockdown effects (6 independent groups) were analyzed with two-way ANOVA. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.