ArticlePloS one2010
CXCR2 signaling protects oligodendrocytes and restricts demyelination in a mouse model of viral-induced demyelination.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Review
- Glial Cells as Key Regulators in Neuroinflammatory Mechanisms Associated with Multiple Sclerosis.International journal of molecular sciences · 2024Review
- Testosterone Inhibits Secretion of the Pro-Inflammatory Chemokine CXCL1 from Astrocytes.Current issues in molecular biology · 2024Article
- Microglia in the context of multiple sclerosis.Frontiers in neurology · 2023Review
- Oligodendrocytes and Microglia: Key Players in Myelin Development, Damage and Repair.Biomolecules · 2021Review
- Treg cell-derived osteopontin promotes microglia-mediated white matter repair after ischemic stroke.Immunity · 2021Article
- A comprehensive review on the role of chemokines in the pathogenesis of multiple sclerosis.Metabolic brain disease · 2021Review
- CXCR2 Signaling and Remyelination in Preclinical Models of Demyelination.DNA and cell biology · 2020Review
- The Role of Chemokines in the Pathogenesis of HTLV-1.Frontiers in microbiology · 2020Review
- Different roles of CXCR1 and CXCR2 in HTLV-1 carriers and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) patients.Medical microbiology and immunology · 2019Article
- Disrupted CXCR2 Signaling in Oligodendroglia Lineage Cells Enhances Myelin Repair in a Viral Model of Multiple Sclerosis.Journal of virology · 2019Article
- Innate Immune Responses and Viral-Induced Neurologic Disease.Journal of clinical medicine · 2018Review
- TRPM2 Exacerbates Central Nervous System Inflammation in Experimental Autoimmune Encephalomyelitis by Increasing Production of CXCL2 Chemokines.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Inflammation-induced Gro1 triggers senescence in neuronal progenitors: effects of estradiol.Journal of neuroinflammation · 2018Article
- Induced CNS expression of CXCL1 augments neurologic disease in a murine model of multiple sclerosis via enhanced neutrophil recruitment.European journal of immunology · 2018Article
- Neutrophils and viral-induced neurologic disease.Clinical immunology (Orlando, Fla.) · 2018Review
- Effect of CXCR2 Inhibition on Behavioral Outcomes and Pathology in Rat Model of Neuromyelitis Optica.Journal of immunology research · 2018Article
- Attempts to Overcome Remyelination Failure: Toward Opening New Therapeutic Avenues for Multiple Sclerosis.Cellular and molecular neurobiology · 2017Review
- MicroRNA-155 enhances T cell trafficking and antiviral effector function in a model of coronavirus-induced neurologic disease.Journal of neuroinflammation · 2016Article
- Inducible Expression of CXCL1 within the Central Nervous System Amplifies Viral-Induced Demyelination.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe functional role of ELR-positive CXC chemokines during viral-induced demyelination was assessed. Inoculation of the neuroattenuated JHM strain of mouse hepatitis virus (JHMV) into the CNS of susceptible mice results in an acute encephalomyelitis that evolves into a chronic demyelinating disease, modeling white matter pathology observed in the human demyelinating disease Multiple Sclerosis. METHODOLOGY/PRINCIPAL
findingsJHMV infection induced the rapid and sustained expression of transcripts specific for the ELR+ chemokine ligands CXCL1 and CXCL2, as well as their binding receptor CXCR2, which was enriched within the spinal cord during chronic infection. Inhibiting CXCR2 signaling with neutralizing antiserum significantly (p<0.03) delayed clinical recovery. Moreover, CXCR2 neutralization was associated with an increase in the severity of demyelination that was independent of viral recrudescence or modulation of neuroinflammation. Rather, blocking CXCR2 was associated with increased numbers of apoptotic cells primarily within white matter tracts, suggesting that oligodendrocytes were affected. JHMV infection of enriched oligodendrocyte progenitor cell (OPC) cultures revealed that apoptosis was associated with elevated expression of cleaved caspase 3 and muted Bcl-2 expression. Inclusion of CXCL1 within JHMV infected cultures restricted caspase 3 cleavage and increased Bcl-2 expression that was associated with a significant (p<0.001) decrease in apoptosis. CXCR2 deficient oligodendrocytes were refractory to CXCL1 mediated protection from JHMV-induced apoptosis, readily activating caspase 3 and down regulating Bcl-2. CONCLUSION/SIGNIFICANCE: These findings highlight a previously unappreciated role for CXCR2 signaling in protecting oligodendrocyte lineage cells from apoptosis during inflammatory demyelination initiated by viral infection of the CNS.
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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.