Cited by 34Neurogenesis and neuroplasticity mechanismsMultiple Sclerosis Research StudiesNeuroinflammation and Neurodegeneration Mechanisms

Myt1L Promotes Differentiation of Oligodendrocyte Precursor Cells and is Necessary for Remyelination After Lysolecithin-Induced Demyelination.

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Shi, Yanqing, Shao, Qi, Li, Zhenghao, Gonzalez, Ginez A., Lu, Fengfeng, Wang, Dan, Pu, Yingyan, Huang, Aijun +3 more·2018·Neuroscience Bulletin

Abstract

The differentiation and maturation of oligodendrocyte precursor cells (OPCs) is essential for myelination and remyelination in the CNS. The failure of OPCs to achieve terminal differentiation in demyelinating lesions often results in unsuccessful remyelination in a variety of human demyelinating diseases. However, the molecular mechanisms controlling OPC differentiation under pathological conditions remain largely unknown. Myt1L (myelin transcription factor 1-like), mainly expressed in neurons, has been associated with intellectual disability, schizophrenia, and depression. In the present study, we found that Myt1L was expressed in oligodendrocyte lineage cells during myelination and remyelination. The expression level of Myt1L in neuron/glia antigen 2-positive (NG2+) OPCs was significantly higher than that in mature CC1+ oligodendrocytes. In primary cultured OPCs, overexpression of Myt1L promoted, while knockdown inhibited OPC differentiation. Moreover, Myt1L was potently involved in promoting remyelination after lysolecithin-induced demyelination in vivo. ChIP assays showed that Myt1L bound to the promoter of Olig1 and transcriptionally regulated Olig1 expression. Taken together, our findings demonstrate that Myt1L is an essential regulator of OPC differentiation, thereby supporting Myt1L as a potential therapeutic target for demyelinating diseases.

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Crossref · 10.1007/s12264-018-0207-9

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Authors
Shi, Y., Shao, Q., Li, Z., Gonzalez, G. A., Lu, F., Wang, D., Pu, Y., Huang, A., Zhao, C., He, C., & Cao, L.
Affiliations
  • Second Military Medical University (CN)
  • Anhui University (CN)
  • Wellcome/MRC Cambridge Stem Cell Institute (GB)
Corresponding author
  • He, Cheng
  • Cao, Li
Venue
Neuroscience Bulletin
Published
2018-02-03
Volume
34
Issue
2
Pages
247-260
ISSN
  • 1995-8218 (ISSN-L)
  • 1673-7067
OpenAlex
W2793262738
Cited by
34
References
44
Citations by year
2026: 1 · 2025: 1 · 2024: 6 · 2023: 5 · 2022: 3 · 2021: 9 · 2020: 6 · 2019: 3
FWCI
1.64
Type
journal article
Language
en
Open access
Locations
  • Neuroscience Bulletin (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Multiple Sclerosis Society
  • Medical Research Council (MR/K008803/1, MR/M010503/1)
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
MYT1L, oligodendrocyte precursor cells, oligodendrocyte differentiation, remyelination, demyelination, lysolecithin-induced demyelination, myelination, demyelinating disease, transcriptional regulation
MeSH terms
Oligodendrocyte Precursor Cells, Remyelination, Animals, Cell Differentiation, Demyelinating Diseases, Lysophosphatidylcholines, Mice, Inbred C57BL, Nerve Tissue Proteins, Oligodendroglia, Transcription Factors, Mice

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