ArticleJournal of neuroinflammation2024
Single-cell sequencing reveals glial cell involvement in development of neuropathic pain via myelin sheath lesion formation in the spinal cord.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Targeting the PDK1/c-Myc/SOX10 Signaling in Oligodendrocytes Alleviates Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Plasma Lipoproteins as Key Regulators in Neuropathic Pain: A Comprehensive Review of Mechanisms and Clinical Potential.Pain and therapy · 2026Review
- Shared Mechanisms and Integrated Management of Post-Stroke Pain and Depression: A Comprehensive Review.Pain and therapy · 2026Review
- Review
- MicroRNA-Mediated Modulation of the Colony-Stimulating Factor 1 Pathway in Microglial Activation and Neuropathic Pain: A Next-Generation Sequencing-Based Transcriptomic Study.Pain research & management · 2026Article
- Single-cell sequencing reveals reversible glial remodeling in the visual cortex during visual deprivation and recovery.Frontiers in immunology · 2026Article
- Microglia Polarization: A Key Regulatory Mechanism of Neuropathic Pain.Journal of pain research · 2026Review
- Multi-Omics Analysis Reveals Nono-Kcnq2 Regulation of Neuronal Excitability in Chronic Constriction Injury-Induced Neuropathic Pain.Research (Washington, D.C.) · 2026Article
- Dysregulation of Hedonic Processing in Chronic Pain: Insights from Preclinical Data.Brain sciences · 2025Review
- Article
- Roles of Ion Channels in Oligodendrocyte Precursor Cells: From Physiology to Pathology.International journal of molecular sciences · 2025Review
- Single-Nucleus Transcriptomics Reveals Glial Metabolic-Immune Rewiring and Intercellular Signaling Disruption in Chronic Migraine.Biomolecules · 2025Article
- Proteomic signatures of type 2 diabetes predict the incidence of coronary heart disease.Cardiovascular diabetology · 2025Article
- Decoding chronic pain: the glutamate-GABA tug of war in the cerebral cortex.Frontiers in molecular neuroscience · 2025Review
- Electroacupuncture Inhibits NLRP3-Mediated Microglial Pyroptosis to Ameliorate Chronic Neuropathic Pain in Rats.Journal of pain research · 2025Article
- Unraveling the emerging role of glial heterogeneity in neuropathic pain: from pathological mechanisms to therapeutic Frontiers.Frontiers in neurologyReview
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Authors and funding
10 authors.
Funding
Abstract
backgroundNeuropathic pain (NP), which results from injury or lesion of the somatosensory nervous system, is intimately associated with glial cells. The roles of microglia and astrocytes in NP have been broadly described, while studies on oligodendrocytes have largely focused on axonal myelination. The mechanisms of oligodendrocytes and their interactions with other glial cells in NP development remain uncertain.
methodsTo explore the function of the interaction of the three glial cells and their interactions on myelin development in NP, we evaluated changes in NP and myelin morphology after a chronic constriction injury (CCI) model in mice, and used single-cell sequencing to reveal the subpopulations characteristics of oligodendrocytes, microglia, and astrocytes in the spinal cord tissues, as well as their relationship with myelin lesions; the proliferation and differentiation trajectories of oligodendrocyte subpopulations were also revealed using pseudotime cell trajectory and RNA velocity analysis. In addition, we identified chemokine ligand-receptor pairs between glial cells by cellular communication and verified them using immunofluorescence.
resultsOur study showed that NP peaked on day 7 after CCI in mice, a time at which myelin lesions were present in both the spinal cord and sciatic nerve. Oligodendrocytes, microglia, and astrocytes subpopulations in spinal cord tissue were heterogeneous after CCI and all were involved in suppressing the process of immune defense and myelin production. In addition, the differentiation trajectory of oligodendrocytes involved a unidirectional lattice process of OPC-1-Oligo-9, which was arrested at the Oligo-2 stage under the influence of microglia and astrocytes. And the CADM1-CADM1, NRP1-VEGFA interactions between glial cells are enhanced after CCI and they had a key role in myelin lesions and demyelination.
conclusionsOur study reveals the close relationship between the differentiation block of oligodendrocytes after CCI and their interaction with microglia and astrocytes-mediated myelin lesions and NP. CADM1/CADM1 and NRP-1/VEGFA may serve as potential therapeutic targets for use in the treatment of NP.
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