ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
NF-κB Activation Protects Oligodendrocytes against Inflammation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 papers.
What it found
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Who cites it
46 citing papers in PubMed, 56 citations in OpenAlex.
- Glial Cysteine Cathepsins: From Homeostasis to Neurodegeneration.Cellular and molecular neurobiology · 2026Review
- Therapeutic Effects of Combined 6-Shogaol and Ibudilast on Neuroinflammation and Behavioral Deficits in a Cuprizone Mouse Model of Multiple Sclerosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Transcriptional Heterogeneity of Oligodendrocytes: Molecular Basis of Diversity Across Development, Brain Regions, and Neurological Diseases.Neurology international · 2026Review
- Oligodendrocytes Are Active Participants in the Pathogenesis of Multiple Sclerosis and Its Animal Models.International journal of molecular sciences · 2026Review
- Exploring the Neuroprotective Role of the Sulfonamide Derivative KM11 in Ethidium Bromide-induced Demyelination in Zebrafish Model Through Modulation of Antioxidant and Inflammatory Cytokine Pathways.Molecular neurobiology · 2025Article
- Curcumin-Piperine Self-Nanoemulsifying Delivery inPharmaceuticals (Basel, Switzerland) · 2025Article
- Enhancer Dynamics and Spatial Organization Drive Anatomically Restricted Cellular States in the Human Spinal Cord.bioRxiv : the preprint server for biology · 2025Article
- Black Seed Oil-Based Curcumin Nanoformulations Ameliorated Cuprizone-Induced Demyelination in the Mouse Hippocampus.Molecular neurobiology · 2025Article
- NF-κB RelA regulates temporal oligodendrocyte differentiation in the postnatal brains.Frontiers in cellular neuroscience · 2025Article
- Review
- pyPAGE: A framework for Addressing biases in gene-set enrichment analysis-A case study on Alzheimer's disease.PLoS computational biology · 2024Article
- Review
- Mechanisms Governing Oligodendrocyte Viability in Multiple Sclerosis and Its Animal Models.Cells · 2024Review
- Reduced Expression of Oligodendrocyte Linage-Enriched Transcripts During the Endoplasmic Reticulum Stress/Integrated Stress Response.ASN neuro · 2024Article
- The PERK pathway: beneficial or detrimental for neurodegenerative diseases and tumor growth and cancer.Human molecular genetics · 2023Review
- Developing Hypoimmunogenic Human iPSC-Derived Oligodendrocyte Progenitor Cells as an Off-The-Shelf Cell Therapy for Myelin Disorders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Article
- NF-κB is a critical mediator of post-mitotic senescence in oligodendrocytes and subsequent white matter loss.Molecular neurodegeneration · 2023Article
- Post-injury born oligodendrocytes incorporate into the glial scar and contribute to the inhibition of axon regeneration.Development (Cambridge, England) · 2023Article
- PLK1 protects intestinal barrier function during sepsis by targeting mitochondrial dynamics through TANK-NF-κB signalling.Molecular medicine (Cambridge, Mass.) · 2022Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
Abstract
NF-κB is a key player in inflammatory diseases, including multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). However, the effects of NF-κB activation on oligodendrocytes in MS and EAE remain unknown. We generated a mouse model that expresses IκBαΔN, a super-suppressor of NF-κB, specifically in oligodendrocytes and demonstrated that IκBαΔN expression had no effect on oligodendrocytes under normal conditions (both sexes). Interestingly, we showed that oligodendrocyte-specific expression of IκBαΔN blocked NF-κB activation in oligodendrocytes and resulted in exacerbated oligodendrocyte death and hypomyelination in young, developing mice that express IFN-γ ectopically in the CNS (both sexes). We also showed that NF-κB inactivation in oligodendrocytes aggravated IFN-γ-induced remyelinating oligodendrocyte death and remyelination failure in the cuprizone model (male mice). Moreover, we found that NF-κB inactivation in oligodendrocytes increased the susceptibility of mice to EAE (female mice). These findings imply the cytoprotective effects of NF-κB activation on oligodendrocytes in MS and EAE.
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Registered trials
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.