ArticleScientific reports2019
Peli1 controls the survival of dopaminergic neurons through modulating microglia-mediated neuroinflammation.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Genetically engineered BMSCs promote dopamine secretion and ameliorate motor dysfunction in a Parkinson's disease rat model.Scientific reports · 2025Article
- RNA mActa neuropsychiatrica · 2024Article
- TonEBP: A Key Transcription Factor in Microglia Following Intracerebral Hemorrhage Induced-Neuroinflammation.International journal of molecular sciences · 2024Article
- The Common Denominators of Parkinson's Disease Pathogenesis and Methamphetamine Abuse.Current neuropharmacology · 2024Review
- The Role of Ubiquitin-Proteasome System and Mitophagy in the Pathogenesis of Parkinson's Disease.Neuromolecular medicine · 2023Review
- Genome-wide association and replication studies for handedness in a Korean community-based cohort.Brain and behavior · 2023Article
- Co-Expression Network Analysis Identifies Molecular Determinants of Loneliness Associated with Neuropsychiatric and Neurodegenerative Diseases.International journal of molecular sciences · 2023Article
- Biology of Pellino1: a potential therapeutic target for inflammation in diseases and cancers.Frontiers in immunology · 2023Review
- Neuroprotective action of α-Klotho against LPS-activated glia conditioned medium in primary neuronal culture.Scientific reports · 2022Article
- The Emerging Roles of Pellino Family in Pattern Recognition Receptor Signaling.Frontiers in immunology · 2022Review
- Duzhong Fang Attenuates the POMC-Derived Neuroinflammation in Parkinsonian Mice.Journal of inflammation research · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic neuroinflammation is known to contributes to the toxicity of neurodegeneration of Parkinson's disease (PD). However, the molecular and cellular mechanisms controlling inflammatory responses in the central nervous system remain poorly understood. Here we found that a E3 ubiquitin ligase Peli1 is dramatically induced only in the substantia nigra (SN) of the human and mouse PD brains. The ablation of Peli1 significantly suppressed LPS-induced production of neurotoxic mediators and proinflammatory cytokines in SN and in primary microglia, whereas Peli1 is dispensable for the inflammatory responses in astrocyte. Accordingly, Peli1 deficiency markedly inhibited neuron death induced by the conditioned medium from LPS-stimulated microglia. Mechanistical study suggested that Peli1 acts as a positive regulator of inflammatory response in microglia through activation of NF-κB and MAP kinase. Our results established Peli1 as a critical mediator in the regulation of microglial activation and neuroinflammation-induced death of dopaminergic neurons during PD pathogenesis, suggesting that targeting Peli1 may have therapeutic effect in neuroinflammation.
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Registered trials
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