DJ-1 inhibits microglial activation and protects dopaminergic neurons in vitro and in vivo through interacting with microglial p65
Open accessAbstract
Parkinson’s disease (PD), one of the most common neurodegenerative disorders, is characterized by progressive neurodegeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). DJ-1 acts essential roles in neuronal protection and anti-neuroinflammatory response, and its loss of function is tightly associated with a familial recessive form of PD. However, the molecular mechanism of DJ-1 involved in neuroinflammation is largely unclear. Here, we found that wild-type DJ-1, rather than the pathogenic L166P mutant DJ-1, directly binds to the subunit p65 of nuclear factor-κB (NF-κB) in the cytoplasm, and loss of DJ-1 promotes p65 nuclear translocation by facilitating the dissociation between p65 and NF-κB inhibitor α (IκBα).DJ-1 knockout (DJ-1−/−) mice exhibit more microglial activation compared with wild-type littermate controls, especially in response to lipopolysaccharide (LPS) treatment. In cellular models, knockdown of DJ-1 significantly upregulates the gene expression and increases the release of LPS-treated inflammatory cytokines in primary microglia and BV2 cells. Furthermore,DJ-1 deficiency in microglia significantly enhances the neuronal toxicity in response to LPS stimulus. In addition, pharmacological blockage of NF-κB nuclear translocation by SN-50 prevents microglial activation and alleviates the damage of DA neurons induced by microglial DJ-1 deficiency in vivo and in vitro. Thus, our data illustrate a novel mechanism by which DJ-1 facilitates the interaction between IκBα and p65 by binding to p65 in microglia, and thus repressing microglial activation and exhibiting the protection of DA neurons from neuroinflammation-mediated injury in PD.
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In microglia, knockdown of DJ-1 enhances production of inflammatory cytokines in response to LPS.
“In microglia, the knockdown of DJ-1 has been shown to enhance the production of inflammatory cytokines in response to LPS.263”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [263]
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Brain organoids as models of extracellular vesicle–mediated human neural communication
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Strategies for Optimizing Genetic Mouse Models to Enhance the Understanding of Parkinson’s Disease
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- Authors
- Lin, Z., Chen, C., Yang, D., Ding, J., Wang, G., & Ren, H.
- Affiliations
- Soochow University (CN)
- Shanghai Jiao Tong University (CN)
- Corresponding author
- Wang, Guanghui
- Ren, Haigang
- Venue
- Cell Death & Disease
- Published
- 2021-07-17
- Volume
- 12
- Issue
- 8
- Pages
- 715-715
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC8286256
- OpenAlex
- W3186026575
- Cited by
- 49
- References
- 55
- Citations by year
- 2026: 4 · 2025: 16 · 2024: 11 · 2023: 10 · 2022: 7 · 2021: 1
- FWCI
- 3.30
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Death and Disease (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (31970966, 32070970)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- DJ-1, Parkinson's disease, microglial activation, dopaminergic neurons, neuroinflammation, NF-κB p65, IκBα, microglia-neuron interaction, LPS-induced neuroinflammation, substantia nigra pars compacta, neuroprotection
- MeSH terms
- Protein Deglycase DJ-1, Animals, Cell Nucleus, Cells, Cultured, Humans, Inflammation, Lipopolysaccharides, Models, Biological, Mutation, Neurotoxins, Protein Binding, Transcription, Genetic, Microglia, Neuroprotective Agents, Protein Subunits, Protein Transport, Mice, Transcription Factor RelA, HEK293 Cells, Dopaminergic Neurons
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