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Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
Published on: September 9, 2022
TRIM37-mediated stabilization of PEX5 via monoubiquitination attenuates oxidative stress and demyelination in
Lai Jiang1,2, Yue Jin2, Yujia Han2
1Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Abstract:
Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS), characterized by myelin damage and neurodegeneration. This study focuses on the role of the TRIM37-PEX5 axis in regulating oxidative stress in oligodendrocytes and myelin repair, exploring its potential as a novel therapeutic target for MS. Through bioinformatics analysis, TRIM37 was found to be significantly downregulated in MS patients. In vitro experiments demonstrated that overexpression TRIM37 could stabilize PEX5 protein via non-degradative monoubiquitination, thereby maintaining peroxisomal metabolic function, reducing oxidative stress levels, significantly decreasing apoptosis in both oligodendrocytes and neurons, and promoting the expression of myelin basic protein (MBP). Further mechanistic studies revealed that the TRIM37-PEX5 axis mitigates apoptosis in oligodendrocytes by regulating oxidative stress levels. in vivo experiments further confirmed the neurorestorative effects of TRIM37. In an experimental autoimmune encephalomyelitis (EAE) model, overexpression TRIM37 significantly suppressed neuroinflammation mediated by microglia, reduced the expression of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), and alleviated demyelination lesions (as evidenced by reduced myelin damage shown by Luxol fast blue (LFB) staining, P < 0.001), while simultaneously increasing MBP expression levels (P < 0.001). In conclusion, targeting the TRIM37-PEX5 axis holds promise as a novel strategy for improving myelin damage and providing neuroprotection in MS, offering a theoretical basis for interventions in metabolism-oxidative stress-related diseases.
Insights
The TRIM37-PEX5 axis shows promise for treating multiple sclerosis (MS). Enhancing TRIM37 protein levels can reduce oxidative stress, protect nerve cells, and promote myelin repair in MS models.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Multiple sclerosis (MS) is a chronic CNS autoimmune disease causing myelin damage and neurodegeneration.
- Oxidative stress and oligodendrocyte dysfunction are key pathological features in MS.
- Identifying novel therapeutic targets is crucial for MS treatment.
Purpose of the Study:
- To investigate the role of the TRIM37-PEX5 axis in oligodendrocyte oxidative stress and myelin repair.
- To explore the therapeutic potential of targeting the TRIM37-PEX5 axis for MS.
Main Methods:
- Bioinformatics analysis to assess TRIM37 expression in MS patients.
- In vitro studies using cell cultures to examine TRIM37 overexpression effects on oligodendrocytes and neurons.
- In vivo studies utilizing an experimental autoimmune encephalomyelitis (EAE) mouse model.
Main Results:
- TRIM37 was downregulated in MS patients.
- TRIM37 overexpression stabilized PEX5, reduced oxidative stress, decreased apoptosis, and promoted myelin basic protein (MBP) expression in vitro.
- In vivo, TRIM37 overexpression suppressed neuroinflammation, reduced pro-inflammatory cytokines (IL-1β, TNF-α), alleviated demyelination, and increased MBP levels in the EAE model.
Conclusions:
- The TRIM37-PEX5 axis plays a critical role in mitigating oxidative stress and apoptosis in oligodendrocytes.
- Targeting the TRIM37-PEX5 axis offers a promising therapeutic strategy for myelin repair and neuroprotection in MS.
- This axis provides a theoretical basis for interventions in metabolism-oxidative stress-related diseases.
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