ArticleNature neuroscience2024
NG2 glia protect against prion neurotoxicity by inhibiting microglia-to-neuron prostaglandin E2 signaling.
Article in Nature neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- NG2-Glia in Central Nervous System Following Injury: From Pathological Involvement to Repair Potential.CNS neuroscience & therapeutics · 2026Review
- Functional Mapping of Neurodevelopmental Disease Pathways to Key Neurodevelopmental Processes Represented in the Developmental Neurotoxicity In Vitro Testing Battery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PrPStem cell reports · 2026Article
- Gpnmb defines a phagocytic state of microglia linked to cell death in prion disease mouse model.Nature communications · 2026Article
- Prostaglandin signaling drives peripheral inflammation-induced reduction of hypothalamic oxytocin-positive neurons.Cellular and molecular life sciences : CMLS · 2026Article
- Alterations in cerebrospinal fluid levels of myelin- and oligodendrocyte-related proteins in sporadic Creutzfeldt-Jakob disease.Acta neuropathologica communications · 2026Article
- Proteoglycans are protagonists in autophagy, lymphangiogenesis, and neurodegenerative diseases.Trends in cell biology · 2026Review
- Multi-omic insight into the molecular mechanism of cuproptosis-related genes in the pathogenesis of Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Mitochondrial microprotein MOCCI controls neuroinflammation by altering glial activation states.Frontiers in immunology · 2026Article
- Tumor-Associated Pericytes: Tumorigenicity and Targeting for Cancer Therapy.Current vascular pharmacology · 2026Review
- Glial Cells in the Early Stages of Neurodegeneration: Pathogenesis and Therapeutic Targets.International journal of molecular sciences · 2025Review
- Impaired macroautophagy in oligodendrocyte precursor cells suppresses neuronal plasticity via a senescence-associated signaling.Science advances · 2025Article
- Multiomic analyses direct hypotheses for Creutzfeldt-Jakob disease risk genes.Brain : a journal of neurology · 2025Article
- Small intestinal γδ T17 cells promote SAE through STING/C1q-induced microglial synaptic pruning in male mice.Nature communications · 2025Article
- Mutant prion protein enhances NMDA receptor activity, activates PKC, and triggers rapid excitotoxicity in mice.The Journal of clinical investigation · 2025Article
- NG2 Glia: The Guardians Against Prion-induced Neurotoxicity Through Prostaglandin E2 Blockade.Neuroscience bulletin · 2025Article
- Role of Glial Cells and Receptors in Schizophrenia Pathogenesis.Neurochemical research · 2025Review
- Role of glial cells in neurotoxicological effects of alcohol.Advances in neurotoxicology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Oligodendrocyte-lineage cells, including NG2 glia, undergo prominent changes in various neurodegenerative disorders. Here, we identify a neuroprotective role for NG2 glia against prion toxicity. NG2 glia were activated after prion infection in cerebellar organotypic cultured slices (COCS) and in brains of prion-inoculated mice. In both model systems, depletion of NG2 glia exacerbated prion-induced neurodegeneration and accelerated prion pathology. Loss of NG2 glia enhanced the biosynthesis of prostaglandin E2 (PGE2) by microglia, which augmented prion neurotoxicity through binding to the EP4 receptor. Pharmacological or genetic inhibition of PGE2 biosynthesis attenuated prion-induced neurodegeneration in COCS and mice, reduced the enhanced neurodegeneration in NG2-glia-depleted COCS after prion infection, and dampened the acceleration of prion disease in NG2-glia-depleted mice. These data unveil a non-cell-autonomous interaction between NG2 glia and microglia in prion disease and suggest that PGE2 signaling may represent an actionable target against prion diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.