ArticleCell death & disease2014
Dock3 protects myelin in the cuprizone model for demyelination.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- VEP Latency Delay Reflects Demyelination Beyond the Optic Nerve in the Cuprizone Model.Investigative ophthalmology & visual science · 2024Article
- Post-injury born oligodendrocytes incorporate into the glial scar and contribute to the inhibition of axon regeneration.Development (Cambridge, England) · 2023Article
- Cuprizone feeding induces swollen astrocyte endfeet.Pflugers Archiv : European journal of physiology · 2022Article
- Validating visual evoked potentials as a preclinical, quantitative biomarker for remyelination efficacy.Brain : a journal of neurology · 2022Article
- Histological and Top-Down Proteomic Analyses of the Visual Pathway in the Cuprizone Demyelination Model.Journal of molecular neuroscience : MN · 2022Article
- Visual Evoked Potentials to Monitor Myelin Cuprizone-Induced Functional Changes.Frontiers in neuroscience · 2022Article
- Catalpol Regulates Oligodendrocyte Regeneration and Remyelination by Activating the GEF-Cdc42/Rac1 Signaling Pathway in EAE Mice.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Oligodendrocyte Lineage Marker Expression in eGFP-GFAP Transgenic Mice.Journal of molecular neuroscience : MN · 2021Article
- Variants in DOCK3 cause developmental delay and hypotonia.European journal of human genetics : EJHG · 2019Article
- Inflammatory demyelination alters subcortical visual circuits.Journal of neuroinflammation · 2017Article
- Retinal Cell Degeneration in Animal Models.International journal of molecular sciences · 2016Review
- Regulating Rac in the nervous system: molecular function and disease implication of Rac GEFs and GAPs.BioMed research international · 2015Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dedicator of cytokinesis 3 (Dock3) belongs to an atypical family of the guanine nucleotide exchange factors. It is predominantly expressed in the neural tissues and causes cellular morphological changes by activating the small GTPase Rac1. We previously reported that Dock3 overexpression protects retinal ganglion cells from excitotoxic cell death. Oligodendrocytes are the myelinating cells of axons in the central nervous system and these cells are damaged in demyelinating disorders including multiple sclerosis (MS) and optic neuritis. In this study, we examined if Dock3 is expressed in oligodendrocytes and if increasing Dock3 signals can suppress demyelination in a cuprizone-induced demyelination model, an animal model of MS. We demonstrate that Dock3 is expressed in oligodendrocytes and Dock3 overexpression protects myelin in the corpus callosum following cuprizone treatment. Furthermore, we show that cuprizone demyelinates optic nerves and the extent of demyelination is ameliorated in mice overexpressing Dock3. Cuprizone treatment impairs visual function, which was demonstrated by multifocal electroretinograms, an established non-invasive method, and Dock3 overexpression prevented this effect. In mice overexpressing Dock3, Erk activation is increased, suggesting this may at least partly explain the observed protective effects. Our findings suggest that Dock3 may be a therapeutic target for demyelinating disorders including optic neuritis.Cell Death and Disease (2014) 5, e1395; doi:10.1038/cddis.2014.357; published online 28 August 2014.
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