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Midbrain dopamine oxidation links ubiquitination of glutathione peroxidase 4 to ferroptosis of dopaminergic neurons
Jie Sun, … , Li Zhang, Rong-Rong He
Jie Sun, … , Li Zhang, Rong-Rong He
Published May 15, 2023
Citation Information: J Clin Invest. 2023;133(10):e165228. https://doi.org/10.1172/JCI165228.
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Research Article Cell biology Neuroscience

Midbrain dopamine oxidation links ubiquitination of glutathione peroxidase 4 to ferroptosis of dopaminergic neurons

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Abstract

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the gradual loss of midbrain dopaminergic neurons in association with aggregation of α-synuclein. Oxidative damage has been widely implicated in this disease, though the mechanisms involved remain elusive. Here, we demonstrated that preferential accumulation of peroxidized phospholipids and loss of the antioxidant enzyme glutathione peroxidase 4 (GPX4) were responsible for vulnerability of midbrain dopaminergic neurons and progressive motor dysfunctions in a mouse model of PD. We also established a mechanism wherein iron-induced dopamine oxidation modified GPX4, thereby rendering it amenable to degradation via the ubiquitin-proteasome pathway. In conclusion, this study unraveled what we believe to be a novel pathway for dopaminergic neuron degeneration during PD pathogenesis, driven by dopamine-induced loss of antioxidant GPX4 activity.

Authors

Jie Sun, Xiao-Min Lin, Dan-Hua Lu, Meng Wang, Kun Li, Sheng-Rong Li, Zheng-Qiu Li, Cheng-Jun Zhu, Zhi-Min Zhang, Chang-Yu Yan, Ming-Hai Pan, Hai-Biao Gong, Jing-Cheng Feng, Yun-Feng Cao, Feng Huang, Wan-Yang Sun, Hiroshi Kurihara, Yi-Fang Li, Wen-Jun Duan, Gen-Long Jiao, Li Zhang, Rong-Rong He

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Figure 3

Phospholipid peroxidation is associated with ferroptosis-associated parkinsonism.

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Phospholipid peroxidation is associated with ferroptosis-associated park...
(A) Schematic diagram showing the study design using 8-month-old A53T transgenic mice treated with low-dose sorafenib (Sora) before measurements. Disordered motor coordination of A53T mice was accelerated by Sora, while the WT mice were unaffected, as displayed by behavioral tests (B) rotarod, (C) pole climbing and (D and E) Catwalk gait analysis (n = 8 mice each group). (F) IHC of coronal brain sections labeled with TH antibody and hematoxylin (left, scale bar: 2 mm). The substantia nigra (dotted area) were amplified on right, scale bar: 500 μm. (G) Western blotting (top) and quantitative analysis (bottom) of TH expression in midbrain. The contents of (H) GSH and (I) MDA were measured in midbrain. (J) Western blotting (left) and quantitative analysis (right) of 4-HNE expression in midbrain. Data of oxidized phospholipids were extracted and displayed as (L) PCA and (K) volcano plots showing the fold changes (X-axis) versus significance (Y-axis) by t-test. (M) Ferroptosis-related genes were detected by quantitative real-time PCR assay and relative expressions displayed as a heatmap. (N) Western blotting (upper) and quantitative analysis (bottom) of GPX4 expression in midbrain (n = 6 mice each group). All data represent mean ± SEM. *P < 0.05, **P < 0.01 and ***P < 0.001, by 1-way ANOVA with Dunnett T3 (for B, C, E, and H) or Bonferroni’s posthoc (for G, I, J, and N) test.

Copyright © 2023 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

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