ArticleBrain : a journal of neurology2015
Fibroblast growth factor signalling in multiple sclerosis: inhibition of myelination and induction of pro-inflammatory environment by FGF9.
Article in Brain : a journal of neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 64 citations in OpenAlex.
- FGFs/FGFRs and neuroinflammatory diseases: mechanism, drug therapies and delivery systems.Journal of advanced research · 2025Review
- Role of Fibroblast Growth Factors in Neurological Disorders: Insight into Therapeutic Approaches and Molecular Mechanisms.Molecular neurobiology · 2025Review
- Review
- Oligodendrocyte-astrocyte crosstalk in Parkinson's disease mediates neuronal ferroptosis via the FGF signaling pathway.NPJ Parkinson's disease · 2025Article
- Demyelination and Remyelination: General Principles.Advances in neurobiology · 2025Review
- LRH-1/NR5A2 targets mitochondrial dynamics to reprogram type 1 diabetes macrophages and dendritic cells into an immune tolerance phenotype.Clinical and translational medicine · 2024Article
- Circulating inflammatory biomarkers and risk of intracranial aneurysm: a Mendelian randomization study.European journal of medical research · 2024Article
- Prognostic value and microenvironmental crosstalk of exosome-related signatures in human epidermal growth factor receptor 2 positive breast cancer.Open life sciences · 2024Article
- The role of fibronectin in multiple sclerosis and the effect of drug delivery across the blood-brain barrier.Neural regeneration research · 2023Review
- Article
- FGF/FGFR system in the central nervous system demyelinating disease: Recent progress and implications for multiple sclerosis.CNS neuroscience & therapeutics · 2023Review
- Interferon Beta-1a versus Combined Interferon Beta-1a and Oligodendrocyte-Specific FGFR1 Deletion in Experimental Autoimmune Encephalomyelitis.International journal of molecular sciences · 2022Article
- Central nervous system regeneration: the roles of glial cells in the potential molecular mechanism underlying remyelination.Inflammation and regeneration · 2022Review
- Human olfactory mesenchymal stromal cell transplantation ameliorates experimental autoimmune encephalomyelitis revealing an inhibitory role for IL16 on myelination.Acta neuropathologica communications · 2022Article
- Natural fish oil improves the differentiation and maturation of oligodendrocyte precursor cells to oligodendrocytesFrontiers in immunology · 2022Article
- Fibroblast Growth Factor Signalling in the Diseased Nervous System.Molecular neurobiology · 2021Review
- Article
- Review
- Oligodendrocyte-specific deletion of FGFR2 ameliorates MOGBrain pathology (Zurich, Switzerland) · 2021Article
- Article
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 4 countries.
Funding
Abstract
Remyelination failure plays an important role in the pathophysiology of multiple sclerosis, but the underlying cellular and molecular mechanisms remain poorly understood. We now report actively demyelinating lesions in patients with multiple sclerosis are associated with increased glial expression of fibroblast growth factor 9 (FGF9), which we demonstrate inhibits myelination and remyelination in vitro. This inhibitory activity is associated with the appearance of multi-branched 'pre-myelinating' MBP+ / PLP+ oligodendrocytes that interact with axons but fail to assemble myelin sheaths; an oligodendrocyte phenotype described previously in chronically demyelinated multiple sclerosis lesions. This inhibitory activity is not due to a direct effect of FGF9 on cells of the oligodendrocyte lineage but is mediated by factors secreted by astrocytes. Transcriptional profiling and functional validation studies demonstrate that these include effects dependent on increased expression of tissue inhibitor of metalloproteinase-sensitive proteases, enzymes more commonly associated with extracellular matrix remodelling. Further, we found that FGF9 induces expression of Ccl2 and Ccl7, two pro-inflammatory chemokines that contribute to recruitment of microglia and macrophages into multiple sclerosis lesions. These data indicate glial expression of FGF9 can initiate a complex astrocyte-dependent response that contributes to two distinct pathogenic pathways involved in the development of multiple sclerosis lesions. Namely, induction of a pro-inflammatory environment and failure of remyelination; a combination of effects predicted to exacerbate axonal injury and loss in patients.
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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.