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Cited by 40Neurogenesis and neuroplasticity mechanismsNuclear Structure and FunctionMultiple Sclerosis Research Studies

Regulation of Myelination in the Central Nervous System by Nuclear Lamin B1 and Non-coding RNAs

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Lin, Shu-Ting, Heng, Mary Y, Ptáček, Louis J, Fu, Ying-Hui·2014·Translational Neurodegeneration
DOI 10.1186/2047-9158-3-4PMC PMC3937061
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Abstract

Adult-onset autosomal dominant leukodystrophy (ADLD) is a progressive and fatal hereditary demyelination disorder characterized initially by autonomic dysfunction and loss of myelin in the central nervous system (CNS). Majority of ADLD is caused by a genomic duplication of the nuclear lamin B1 gene (LMNB1) encoding lamin B1 protein, resulting in increased gene dosage in brain tissue. In vitro, excessive lamin B1 at the cellular level reduces transcription of myelin genes, leading to premature arrest of oligodendrocyte differentiation. Murine models of ADLD overexpressing LMNB1 exhibited age-dependent motor deficits and myelin defects, which are associated with reduced occupancy of the Yin Yang 1 transcription factor at the promoter region of the proteolipid protein gene. Lamin B1 overexpression mediates oligodendrocyte cell-autonomous neuropathology in ADLD and suggests lamin B1 as an important regulator of myelin formation and maintenance during aging. Identification of microRNA-23 (miR-23) as a negative regulator of lamin B1 can ameliorate the consequences of excessive lamin B1 at the cellular level. miR-23a-overexpressing mice display enhanced oligodendrocyte differentiation and myelin synthesis. miR-23a targets include a protein coding transcript PTEN (phosphatase and tensin homolog on chromosome 10), and a long noncoding RNA (2700046G09Rik), indicating a unique role for miR-23a in the coordination of proteins and noncoding RNAs in generating and maintaining healthy myelin. Here, we provide a concise review of the current literature on clinical presentations of ADLD and how lamin B1 affects myelination and other developmental processes. Moreover, we address the emerging role of non-coding RNAs (ncRNAs) in modulating gene networks, specifically investigating miR-23 as a potential target for the treatment of ADLD and other demyelinating disorders.

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  • miR-23a can inhibit expression of lamin B1 to protect against leukodystrophy characterized by demyelination of the central nervous system.

    “it can inhibit the expression of lamin B1 to protect against leukodystrophy characterized by demyelination of the central nervous system.”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [133]

    The section on miRNA-23 regulation of myelination (page unavailable) says miR-23a represses lamin B1 and that miR-23 can counteract lamin B1’s adverse effects in oligodendrocyte cells. The review describes miR-23 as a potential treatment target for ADLD, but does not show that it protects against leukodystrophy in affected organisms or patients. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Overexpressing miR-23a in mice was observed as the thickness of myelin increases.

    “overexpressing miR-23a in mice was observed as the thickness of myelin increases”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [133]

  • LncRNA 2700046G09Rik was targeted by miR-23a to modulate PTEN and maintain normal myelin function.

    “LncRNA 2700046G09Rik was targeted by miR-23a to modulate phosphatase and tensin homolog and maintain normal myelin function [133,134].”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [133]

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Authors
Lin, S.-T., Heng, M. Y., Ptáček, L. J., & Fu, Y.-H.
Affiliations
  • University of California, San Francisco (US)
  • Howard Hughes Medical Institute (US)
Corresponding author
Fu, Ying-Hui
ORCID
Venue
Translational Neurodegeneration
Publisher
Springer Science and Business Media LLC
Published
2014-02-05
Volume
3
Issue
1
Pages
4-4
ISSN
2047-9158 (ISSN-L)
DOI
10.1186/2047-9158-3-4
PMC
PMC3937061
OpenAlex
W2108515285
Cited by
40
References
97
Citations by year
2025: 1 · 2024: 5 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 5 · 2019: 4 · 2018: 5 · 2017: 5 · 2016: 6 · 2015: 4 · 2014: 1
FWCI
1.86
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Translational Neurodegeneration (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
  • Howard Hughes Medical Institute
  • National Institutes of Health
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
Keywords
lamin B1, myelination, demyelination, oligodendrocyte differentiation, myelin genes, proteolipid protein, microRNA-23a, PTEN, long non-coding RNA, non-coding RNA, demyelinating disease, gene therapy

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