Cited by 99Neurogenesis and neuroplasticity mechanismsMultiple Sclerosis Research StudiesMesenchymal stem cell research

Mechanisms of oligodendrocyte regeneration from ventricular-subventricular zone-derived progenitor cells in white matter diseases

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Maki, Takakuni, Liang, Anna C., Miyamoto, Nobukazu, Lo, Eng H., Arai, Ken·2013·Frontiers in Cellular Neuroscience

Abstract

White matter dysfunction is an important part of many CNS disorders including multiple sclerosis (MS) and vascular dementia. Within injured areas, myelin loss and oligodendrocyte death may trigger endogenous attempts at regeneration. However, during disease progression, remyelination failure may eventually occur due to impaired survival/proliferation, migration/recruitment, and differentiation of oligodendrocyte precursor cells (OPCs). The ventricular-subventricular zone (V-SVZ) and the subgranular zone (SGZ) are the main sources of neural stem/progenitor cells (NSPCs), which can give rise to neurons as well as OPCs. Under normal conditions in the adult brain, the V-SVZ progenitors generate a large number of neurons with a small number of oligodendrocyte lineage cells. However, after demyelination, the fate of V-SVZ-derived progenitor cells shifts from neurons to OPCs, and these newly generated OPCs migrate to the demyelinating lesions to ease white matter damage. In this mini-review, we will summarize the recent studies on extrinsic (e.g., vasculature, extracellular matrix (ECM), cerebrospinal fluid (CSF)) and intrinsic (e.g., transcription factors, epigenetic modifiers) factors, which mediate oligodendrocyte generation from the V-SVZ progenitor cells. A deeper understanding of the mechanisms that regulate the fate of V-SVZ progenitor cells may lead to new therapeutic approaches for ameliorating white matter dysfunction and damage in CNS disorders.

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  • These previously uncharacterized temporal modules comprised oligodendrocyte lineage progression TFs and co-expression partners.

    “These previously uncharacterized temporal modules comprised oligodendrocyte lineage progression TFs (e.g., Kcnip3, Olig2, Sox2, and Klf9; Maki et al., 2013; Marques et al., 2016; Tokumoto et al., 2017; Wu et al., 2012) and co-expression partners (e.g., Hes5, Eno1, Sox21, Purb, Zfp275, Foxj2, Zeb2, Tsc22d3, and Hopx; Figure 4F).”

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Authors
Maki, T., Liang, A. C., Miyamoto, N., Lo, E. H., & Arai, K.
Affiliations
Harvard University (US)
Corresponding author
Arai, Ken
Venue
Frontiers in Cellular Neuroscience
Published
2013
Volume
7
Pages
275-275
ISSN
1662-5102 (ISSN-L)
OpenAlex
W2161807158
Cited by
99
References
123
Citations by year
2026: 2 · 2025: 4 · 2024: 5 · 2023: 8 · 2022: 4 · 2021: 9 · 2020: 7 · 2019: 11 · 2018: 8 · 2017: 10 · 2016: 16 · 2015: 7 · 2014: 8
FWCI
1.10
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health
  • National Institute of Neurological Disorders and Stroke (R01NS065089)
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
Keywords
oligodendrocyte regeneration, ventricular-subventricular zone, neural stem/progenitor cells, oligodendrocyte precursor cells, white matter disease, remyelination failure, demyelination, multiple sclerosis, vascular dementia, subgranular zone, transcription factors, epigenetic regulators, extracellular matrix, cerebrospinal fluid, vascular system

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