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Page 57 Plössl et al. J Transl Genet Genom 2022;6:46-62 https://dx.doi.org/10.20517/jtgg.2021.39

Figure 5. SI-mediated oxidative stress in iPSC-RPE after 72 h treatment. iPSC-RPE cell lines were treated daily with fresh 0.125 or
0.25 mM SI for a total of 72 h, cells incubated in medium without SI served as a control. mRNA expression of HMOX1 (A) and NQO1 (B)
was determined via quantitative reverse transcriptase polymerase chain reaction after normalization to HPRT1 and calibration against
the control (ctrl). While SI treatment significantly upregulated both NQO1 and HMOX1 expression, no differences in the NRF2 mediated
stress response could be observed between HR and LR lines. Western blot analyses using antibodies against HMOX1 and NQO1 (C, D).
Signal intensities were normalized against ACTB as a loading control and calibrated against the untreated control. Data are presented
as means + SD [n = 3 for (A, B) and n = 4 for (C, D)] for left panels showing individual cell lines, while n = 4 for comparison between HR
and LR; *P < 0.05, Mann-Whitney U-test. SI: Sodium iodate; iPSC: induced pluripotent stem cell; RPE: retinal pigment epithelium; HR:
high-risk; LR: low-risk.

to suggest that NRF2-dependent oxidative stress response following artificial stress induction by application
of SI in RPE cells is not dependent to a measurable extent on genetic AMD susceptibility.

Monogenetic disorders are commonly caused by variants in a few genes while the causal variants usually
display strong effects on the phenotypic expression. This makes it rather straightforward to model