ArticleBrain research2007
Diminished cytokine and chemokine expression in the central nervous system of GMF-deficient mice with experimental autoimmune encephalomyelitis.
Article in Brain research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- The role of actin cytoskeleton component Arp2/3 in inflammatory response.Frontiers in cell and developmental biology · 2025Review
- Glia Maturation Factor (GMF) Regulates Microglial Expression Phenotypes and the Associated Neurological Deficits in a Mouse Model of Traumatic Brain Injury.Molecular neurobiology · 2020Article
- Neuroinflammation Mediated by Glia Maturation Factor Exacerbates Neuronal Injury in anJournal of neurotrauma · 2020Article
- Brain Injury-Mediated Neuroinflammatory Response and Alzheimer's Disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2020Review
- Potential role of poly (ADP-ribose) polymerase in delayed cerebral vasospasm following subarachnoid hemorrhage in rats.Experimental and therapeutic medicine · 2019Article
- GMF as an Actin Network Remodeling Factor.Trends in cell biology · 2018Review
- Glia Maturation Factor and Mast Cell-Dependent Expression of Inflammatory Mediators and Proteinase Activated Receptor-2 in Neuroinflammation.Journal of Alzheimer's disease : JAD · 2018Article
- Glia maturation factor-β: a potential therapeutic target in neurodegeneration and neuroinflammation.Neuropsychiatric disease and treatment · 2018Review
- First description of enhanced expression of glia maturation factor-beta in experimental toxoplasmic encephalitis.The Journal of international medical research · 2017Article
- Mast Cell Activation in Brain Injury, Stress, and Post-traumatic Stress Disorder and Alzheimer's Disease Pathogenesis.Frontiers in neuroscience · 2017Review
- Glia Maturation Factor and Mitochondrial Uncoupling Proteins 2 and 4 Expression in the Temporal Cortex of Alzheimer's Disease Brain.Frontiers in aging neuroscience · 2017Article
- Absence of glia maturation factor protects dopaminergic neurons and improves motor behavior in mouse model of parkinsonism.Neurochemical research · 2015Article
- Resolution of central nervous system astrocytic and endothelial sources of CCL2 gene expression during evolving neuroinflammation.Fluids and barriers of the CNS · 2014Article
- Glia maturation factor expression in entorhinal cortex of Alzheimer's disease brain.Neurochemical research · 2013Article
- Glia maturation factor expression in hippocampus of human Alzheimer's disease.Neurochemical research · 2013Article
- Immune privilege as an intrinsic CNS property: astrocytes protect the CNS against T-cell-mediated neuroinflammation.Mediators of inflammation · 2013Review
- Enhanced expression of glia maturation factor correlates with glial activation in the brain of triple transgenic Alzheimer's disease mice.Neurochemical research · 2013Article
- Efficient down-regulation of glia maturation factor expression in mouse brain and spinal cord.Neurochemical research · 2012Article
- Clinical course of myelin oligodendrocyte glycoprotein 35-55 induced experimental autoimmune encephalomyelitis is aggravated by glia maturation factor.Neurochemistry international · 2012Article
- Innate-adaptive crosstalk: how dendritic cells shape immune responses in the CNS.Advances in experimental medicine and biology · 2012Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Pro-inflammatory cytokines/chemokines are implemented in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model with clinical and pathological similarities to multiple sclerosis. We have previously shown that over-expression of glia maturation factor (GMF) in glial cells cause excessive production and secretion of pro-inflammatory cytokines/chemokines sufficient to destroy the myelin-forming oligodendroglial cell in vitro. In this present investigation, we evaluate the expression of pro-inflammatory mediators in the central nervous system (CNS) of GMF+/+ (wild type) mice and GMF-/- (GMF-knockout) mice at the peak of EAE induced by immunization with MOG 35-55 peptide. GMF+/+ (Wt) mice developed severe EAE with a maximal mean clinical score of 3.6+/-0.5 by day 16 post-immunization, whereas GMF-KO mice showed significantly delayed EAE with an average onset on day 26 pi with reduced mean clinical score of 1.3+/-0.3. Three of fifteen Wt mice as compared to none of GMF-KO mice died of EAE. Encephalitogenic cells from Wt mice transferred to recipient GMF-KO mice caused very mild and with low incidence of EAE. We determined the differences in the expression of cytokines, IFN-gamma, TNF-alpha, IL-1 beta, IL-6, IL-4, IL-10, and chemokines, MIP-1, MIP-2, IP-10, MCP-1, GM-CSF mRNA by quantitative real-time RT-PCR in brain and spinal cord. Our results demonstrate significantly low levels of pro-inflammatory cytokines/chemokines in the CNS of GMF-KO mice and increased expression in Wt mice with EAE. Our data suggest that GMF play a critical role in CNS inflammation.
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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.