About: Fibroblast growth factor 2 (FGF2) and FGF receptor expression in an experimental demyelinating disease with extensive remyelination

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About: Fibroblast growth factor 2 (FGF2) and FGF receptor expression in an experimental demyelinating disease with extensive remyelination Goto Sponge NotDistinct Permalink

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

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Fibroblast growth factor 2 (FGF2) and FGF receptor expression in an experimental demyelinating disease with extensive remyelination
Creator	Armstrong, Regina Le, Tuan Messersmith, Donna Frost, Emma Murtie, Joshua
Source	Medline; PMC
abstract	Fibroblast growth factor 2 (FGF2) is an excellent candidate to regulate remyelination based on its proposed actions in oligodendrocyte lineage cell development in conjunction with its involvement in CNS regeneration. To assess the potential for FGF2 to play a role in remyelination, we examined the expression pattern of FGF2 and FGF receptors (FGFRs) in an experimental demyelinating disease with extensive remyelination. Adult mice were intracranially injected with murine hepatitis virus strain A‐59 (MHV‐A59) to induce focally demyelinated spinal cord lesions that spontaneously remyelinate, with corresponding recovery of motor function. Using kinetic RT‐PCR analysis of spinal cord RNA, we found significantly increased levels of FGF2 mRNA transcripts, which peaked during the initial stage of remyelination. Analysis of tissue sections demonstrated that increased levels of FGF2 mRNA and protein were localized within demyelinated regions of white matter, including high FGF2 expression associated with astrocytes. The expression of corresponding FGF receptors was significantly increased in lesion areas during the initial stage of remyelination. In normal and lesioned white matter, oligodendrocyte lineage cells, including progenitors and mature cells, were found to express multiple FGFR types (FGFR1, FGFR2, and/or FGFR3). In addition, in lesion areas, astrocytes expressed FGFR1, FGFR2, and FGFR3. These findings indicate that, during remyelination, FGF2 may play a role in directly regulating oligodendrocyte lineage cell responses and may also act through paracrine or autocrine effects on astrocytes, which are known to synthesize other growth factors and immunoregulatory molecules that influence oligodendrocyte lineage cells. J. Neurosci. Res. 62:241–256, 2000. Published 2000 Wiley‐Liss, Inc.
has issue date	2000-09-29(xsd:dateTime)
bibo:doi	10.1002/1097-4547(20001015)62:2<241::aid-jnr9>3.0.co;2-d
bibo:pmid	11020217
has license	no-cc
sha1sum (hex)	3bbd50e7592ed9e301ee45cec6d881ca07fabf5d
schema:url	https://doi.org/10.1002/1097-4547%2820001015%2962:2%3C241::aid-jnr9%3E3.0.co%3B2-d
resource representing a document's title	Fibroblast growth factor 2 (FGF2) and FGF receptor expression in an experimental demyelinating disease with extensive remyelination
has PubMed Central identifier	PMC7138084
has PubMed identifier	11020217
schema:publication	J Neurosci Res
resource representing a document's body	covid:3bbd50e7592ed9e301ee45cec6d881ca07fabf5d#body_text
is schema:about of	named entity 'development' named entity 'FGFR3' named entity 'receptors' named entity 'regeneration' named entity 'injected' named entity 'astrocytes' named entity 'induce' named entity 'motor function' named entity 'Disease' named entity 'Fibroblast Growth Factor' named entity 'cells' named entity 'tissue' named entity 'multiple' named entity 'FGF2' named entity 'demonstrated' named entity 'expression' named entity 'FGF2' named entity 'spinal cord' named entity 'FGFR' named entity 'spontaneously' named entity 'addition' named entity 'influence' named entity 'spinal cord' named entity 'FGFR2' named entity 'FGFR3' named entity 'growth factors' named entity 'astrocytes' named entity 'FGF2' named entity 'CNS' named entity 'mRNA' named entity 'FGF2' named entity 'FGF2' named entity 'FGFR1' named entity 'hepatitis virus' named entity 'tissue sections' named entity 'astrocytes' named entity 'oligodendrocyte' named entity 'FGF2' named entity 'mice' named entity 'remyelination' named entity 'oligodendrocyte' named entity 'spinal cord lesions' named entity 'FGFR' named entity 'Receptor Expression' named entity 'FGF2' named entity 'oligodendrocytes' named entity 'FGF2' named entity 'mRNA' named entity 'gray matter' named entity 'Remyelination' named entity 'RNA' named entity 'FGFR1' named entity 'Bjugn' named entity 'demyelination' named entity 'motor function' named entity 'remyelination' named entity 'primers' named entity 'FGFR1' named entity 'mRNA' named entity 'cytoplasm' named entity 'FGFR3' named entity 'FGFR3' named entity 'spinal cord' named entity 'FGFR3' named entity 'FGF2' named entity 'FGF2' named entity 'FGFR3' named entity 'FGFR3' named entity 'immunoreactivity' named entity 'demyelination' named entity 'RT-PCR' named entity 'vacuolated' named entity 'immunostaining' named entity 'FGF2' named entity 'immunoreactivity' named entity 'perinuclear' named entity 'mice'

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