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pLG72 induces superoxide radicals via interaction and aggregation with SOD1
Maofeng Wang1, Hean-Pat Saw2,3, Fei-Fei Cui1
1a Department of Biomedical Science Laboratory , Affiliated Dongyang Hospital of Wenzhou Medical University , Dongyang , Zhejiang , China.
Free Radical Research
|July 25, 2018
Summary
The G72 gene product, pLG72, induces superoxide radicals and impairs SOD1 function, leading to reduced cell proliferation. This mechanism may contribute to neurodegenerative diseases like schizophrenia.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- G72 is a susceptibility gene implicated in neurodegenerative diseases such as schizophrenia and major depression.
- Its product, pLG72, is a potential serum biomarker for schizophrenia.
- Previous studies suggest pLG72 may induce mitochondrial reactive oxygen species (ROS), causing cell damage.
Purpose of the Study:
- To investigate the mechanism by which pLG72 affects cellular processes.
- To determine the specific type of ROS induced by pLG72.
- To explore the interaction of pLG72 with key cellular components.
Main Methods:
- Transfection of a human U87 glioblastoma cell line with a G72 construct.
- Use of ROS-specific scavengers to identify induced radicals.
- Co-localization studies to investigate protein interactions.
- Measurement of superoxide dismutase (SOD) activity and cell proliferation.
Main Results:
- Superoxide radicals were specifically induced in pLG72-expressing cells.
- pLG72 interacted and co-localized with superoxide dismutase 1 (SOD1).
- SOD1 aggregation led to a significant reduction in total SOD activity (23-74%) and a 29% decrease in cell proliferation.
Conclusions:
- pLG72 induces superoxide radicals and impairs SOD1 function, leading to decreased cell proliferation.
- The observed loss of SOD1 function by pLG72 may explain elevated ROS levels and inhibited cell growth.
- This mechanism has implications for understanding the pathogenesis of neurodegenerative diseases.
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