About: Fibroblast growth factor signalling in multiple sclerosis: inhibition of myelination and induction of pro-inflammatory environment by FGF9

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About: Fibroblast growth factor signalling in multiple sclerosis: inhibition of myelination and induction of pro-inflammatory environment by FGF9 Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Fibroblast growth factor signalling in multiple sclerosis: inhibition of myelination and induction of pro-inflammatory environment by FGF9
Creator	Lassmann, Hans Linington, Christopher Schuh, Cornelia Barnett, Susan Williams, Anna Stadelmann, Christine Meinl, Edgar Arthur, Ariel Brunner, Sarah Edgar, Julia Elliott, Christina Glasgow, Lindner, Maren Mcelroy, Daniel Mohan, Hema Mudaliar, Manikhandan Mü, Steve Schaeren-Wiemers, Nicole Thü, Katja
Source	PMC
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.
has issue date	2015-04-23(xsd:dateTime)
bibo:doi	10.1093/brain/awv102
bibo:pmid	25907862
has license	no-cc
sha1sum (hex)	b6af5340202e9e22924da7fdb0c7b8ad173dfac4
schema:url	https://doi.org/10.1093/brain/awv102
resource representing a document's title	Fibroblast growth factor signalling in multiple sclerosis: inhibition of myelination and induction of pro-inflammatory environment by FGF9
has PubMed Central identifier	PMC7185739
has PubMed identifier	25907862
schema:publication	Brain
resource representing a document's body	covid:b6af5340202e9e22924da7fdb0c7b8ad173dfac4#body_text
is schema:about of	named entity 'signalling' named entity 'FGF9' named entity 'environment' named entity 'pro-inflammatory' named entity 'myelination' named entity 'FGF9' named entity 'rat' named entity 'FGF9' named entity '3-amino-9-ethylcarbazole' named entity 'insulin' named entity 'FGF9' named entity 'Cd44' named entity 'disintegrin' named entity 'oligodendrocytes' named entity 'TIMP2' named entity 'Jak-STAT' named entity 'FGF9' named entity 'streptomycin' named entity 'chemokine' named entity 'digoxigenin' named entity 'FGF9' named entity 'oligodendrocytes' named entity 'astrocytes' named entity 'hydrogen peroxide' named entity 'FGF9' named entity 'MMP1' named entity 'T7 RNA polymerase' named entity 'FGFR' named entity 'Immunocytochemistry' named entity 'myelination' named entity 'ZEB2' named entity 'FGF9' named entity 'FGF9' named entity 'Invitrogen' named entity 'Papain' named entity 'white matter' named entity 'oligodendrocytes' named entity 'morphologically' named entity 'vasculature' named entity 'ABC' named entity 'lesion' named entity 'lesions' named entity 'FGF9' named entity 'multiple sclerosis' named entity 'FGF9' named entity 'lesion' named entity 'data analysis' named entity 'MBP' named entity 'remyelination' named entity 'primary antibodies' named entity 'immunoreactivity' named entity 'MMP' named entity 'NG2' named entity 'reverse transcription' named entity 'RNA' named entity 'Binding Site' named entity 'neurosphere' named entity 'Miltenyi Biotec' named entity 'repair mechanism' named entity 'antibody' named entity 'proinflammatory' named entity 'embryonic Day' named entity 'immunoreactive'

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