Fig. 5: Forced expression of ATP6V0A2 mitigates ferroptosis in cardiomyocytes and murine hearts. | Cell Death Discovery

Fig. 5: Forced expression of ATP6V0A2 mitigates ferroptosis in cardiomyocytes and murine hearts.

From: Epirubicin induces cardiotoxicity through disrupting ATP6V0A2-dependent lysosomal acidification and triggering ferroptosis in cardiomyocytes

Fig. 5

HL-1 cardiomyocytes were transfected with plasmids of scramble or ATP6V0A2 in advance, and then treated with DMSO or EPI (2 μM) for 12 h. The mRNA levels of PTGS2 (A) and NOX1 (B) in HL-1 cardiomyocytes in the indicated groups. C–F Immunoblotting analysis of PTGS2, NOX1 and GPX4 proteins of HL-1 cardiomyocytes in the indicated groups. G, H DCFH-DA probe was used to detect the relative ROS level of HL-1cardiomyocytes in the indicated groups flow cytometry and the quantitative analysis of DCF (FL1) fluorescence are shown. I, J BODIPY581/591-C11 probe was used to detected lipid peroxidation level in HL-1 cardiomyocytes treated with indicated chemicals by flow cytometry and the quantitative analysis of BODIPY581/591 -C11 (FL1) fluorescence are shown. K The relative GSH level of HL-1 cardiomyocytes was detected in the indicated groups. L–N The protein abundance of PTGS2 and NOX1 in murine hearts in the indicated groups. n = 3 mice per group. O Representative images of transmission electron microscopy show morphology of the mitochondrion. Scale bars are shown in the images. One-way ANOVA followed by the Tukey post hoc test was used to compare indicated treatment groups and control group in murine hearts. Two-way ANOVA and subsequent Tukey test was performed to compare groups with different secondary treatments in HL-1 cells. ***p < 0.001, **p < 0.01, *p < 0.05.

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