Cited by 157Neurogenesis and neuroplasticity mechanismsMultiple Sclerosis Research StudiesMesenchymal stem cell research

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PDGF and FGF2 pathways regulate distinct oligodendrocyte lineage responses in experimental demyelination with spontaneous remyelination

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Murtie, Joshua C., Zhou, Yong-Xing, Le, Tuan Q., Vana, Adam C., Armstrong, Regina C.·2005·Neurobiology of Disease

DOI 10.1016/j.nbd.2004.12.006

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Abstract

Repair of myelin damage in the adult CNS requires oligodendrocyte progenitor (OP) proliferation and subsequent differentiation into remyelinating oligodendrocytes. Platelet-derived growth factor (PDGF) and fibroblast growth factor-2 (FGF2) have been predicted to act individually and/or cooperatively to generate remyelinating oligodendrocytes. Analysis of PDGF alpha receptor (PDGF alpha R) heterozygous (+/-) mice indicates that PDGF alpha R expression modulates oligodendrocyte density in non-lesioned adult CNS. Analysis of cuprizone demyelination and recovery in PDGF alpha R+/- mice, FGF2 knockout (-/-) mice, and PDGF alpha R+/- FGF2-/- mice demonstrated that: (1) OP proliferation and oligodendrocyte regeneration is impaired in PDGF alpha R heterozygotes, (2) PDGF alpha R+/- and FGF2-/- deletions do not act cooperatively to impair OP amplification, (3) oligodendrocyte differentiation is more frequent in FGF2-/- mice, and (4) FGF2 deletion in combination with the PDGF alpha R+/- genotype rescues impaired oligodendrocyte regeneration of PDGF alpha R heterozygotes. These findings demonstrate distinct roles for PDGF and FGF2 in vivo in the context of a demyelinating disease with spontaneous remyelination.

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Authors: Murtie, J. C., Zhou, Y.-X., Le, T. Q., Vana, A. C., & Armstrong, R. C.
Affiliations: Uniformed Services University of the Health Sciences (US)
Corresponding author: Armstrong, Regina C.
ORCID: Armstrong, Regina C.
Venue: Neurobiology of Disease
Publisher: Elsevier BV
Published: 2005-06
Volume: 19
Issue: 1-2
Pages: 171-182
ISSN: 0969-9961 (ISSN-L)
DOI: 10.1016/j.nbd.2004.12.006
OpenAlex: W2021786345
Cited by: 157
References: 50
Citations by year: 2026: 3 · 2025: 5 · 2024: 9 · 2023: 5 · 2022: 4 · 2021: 5 · 2020: 6 · 2019: 9 · 2018: 7 · 2017: 3 · 2016: 10 · 2015: 11 · 2014: 14 · 2013: 12 · 2012: 8
FWCI: 2.29
Type: journal article
Language: en
Open access: green
doaj.org
Licence: cc-by-sa
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neurobiology of Disease (publishedVersion)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: National Institute of Neurological Disorders and Stroke (R01NS039293, NS39293)
Topics: Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Mesenchymal stem cell research
Keywords: platelet-derived growth factor, fibroblast growth factor 2, PDGF receptor alpha, oligodendrocyte precursor cells, remyelination, demyelination, cuprizone, oligodendrocyte differentiation, oligodendrocyte proliferation
MeSH terms: Animals, Corpus Callosum, Demyelinating Diseases, Male, Mice, Inbred C57BL, Nerve Fibers, Myelinated, Oligodendroglia, Signal Transduction, Fibroblast Growth Factor 2, Mice, Knockout, Cell Lineage, Receptor, Platelet-Derived Growth Factor alpha, NIH 3T3 Cells, Mice

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PDGF and FGF2 pathways regulate distinct oligodendrocyte lineage responses in experimental demyelination with spontaneous remyelination

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