ArticleThe American journal of pathology1998
Experimental autoimmune encephalomyelitis in mice lacking glial fibrillary acidic protein is characterized by a more severe clinical course and an infiltrative central nervous system lesion.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Astrocytes in Multiple Sclerosis: Getting to the Core.International journal of molecular sciences · 2026Review
- Astrocyte CBJournal of neuroinflammation · 2026Article
- Astrocytic-OTUD7B ameliorates murine experimental autoimmune encephalomyelitis by stabilizing glial fibrillary acidic protein and preventing inflammation.Nature communications · 2025Article
- Innate Immunity in the Pathogenesis of Selected Autoimmune Neurological Diseases.Journal of clinical medicine · 2025Review
- Article
- Improved immunostaining of nanostructures and cells in human brain specimens through expansion-mediated protein decrowding.Science translational medicine · 2024Article
- Panaxcerol D fromJournal of ginseng research · 2024Article
- Effects of 660-nm LED photobiomodulation on drebrin expression pattern and astrocyte migration.Scientific reports · 2023Article
- Potential biological contributers to the sex difference in multiple sclerosis progression.Frontiers in immunology · 2023Article
- Chemogenetic manipulation of astrocyte activity at the synapse- a gateway to manage brain disease.Frontiers in cell and developmental biology · 2023Review
- Central nervous system demyelinating diseases: glial cells at the hub of pathology.Frontiers in immunology · 2023Review
- Function and therapeutic value of astrocytes in neurological diseases.Nature reviews. Drug discovery · 2022Review
- Repurposing cancer drugs identifies kenpaullone which ameliorates pathologic pain in preclinical models via normalization of inhibitory neurotransmission.Nature communications · 2021Article
- Review
- GFAP (Glial Fibrillary Acidic Protein)-Positive Progenitor Cells Contribute to the Development of Vascular Smooth Muscle Cells and Endothelial Cells-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Neuroprotective Potential ofNutrients · 2020Article
- Effect of acute pentylenetetrazol injection induced epileptic seizures on rat dentate gyrus at different postnatal ages.Anatomy & cell biology · 2020Article
- The contribution of astrocytes to the neuroinflammatory response in multiple sclerosis and experimental autoimmune encephalomyelitis.Acta neuropathologica · 2019Review
- Resistin-Inhibited Neural Stem Cell-Derived Astrocyte Differentiation Contributes to Permeability Destruction of the Blood-Brain Barrier.Neurochemical research · 2019Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Insights into the role of the astrocyte intermediate filament protein, glial fibrillary acidic protein (GFAP), have only recently emerged with reports on subtle abnormalities in GFAP-deficient mice, including the documentation of defective long-term maintenance of central nervous system myelination. Here, we extend these observations by examining the astroglial response in GFAP-/- mice with autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. Clinically, the monophasic disease was more severe in GFAP-/- mice than in wild-type littermates despite increased remyelination in the former. More in keeping with the clinical course was the observation of an infiltrative EAE lesion in GFAP-/- mice. GFAP-/- astrocytes had a reduced cytoarchitectural stability as evidenced by less abundant and irregularly spaced hemidesmosomes. The blunt GFAP-/- astrocyte processes possessed intermediate filaments consisting mainly of vimentin, though to a lesser degree than in the wild-type. In contrast, in wild-type littermates, GFAP was most abundant and nestin occurred at lower levels. Taken together, the present study introduces the novel concepts that GFAP plays an important role in the control of clinical disease associated with formation of a clearly defined edge to the EAE lesion and that GFAP is operative in the regulation of the intermediate filament components in reactive fibrillary astrogliosis.
Indexed as
Identifiers
9422542PMC1858102What OpenQuestion holds
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.