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PDGF and FGF2 pathways regulate distinct oligodendrocyte lineage responses in experimental demyelination with spontaneous remyelination
Open accessAbstract
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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“Another study showed an impaired oligodendrocyte repopulation in PDGFαR heterozygous knockout mice, caused by a reduced proliferation capacity and overall density of OPC arguing for an important role of PDGFαR-signaling on OPC proliferation.”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Murtie et al., 2005b
In the citing paper
“arguing for an important role of PDGFαR-signaling on OPC proliferation.”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Murtie et al., 2005b
In the citing paper
“Differentiation of OPC was, however, not altered in PDGFαR +/− mice (Murtie et al., 2005b).”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Murtie et al., 2005b
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Metadata
- 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)
- 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
- 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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