ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Loss of branched O-mannosyl glycans in astrocytes accelerates remyelination.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Branching of O-mannose glycans regulates node of Ranvier organization and saltatory conduction.Communications biology · 2026Article
- Enzymatic basis of branching and extension of O-Man glycans for keratan sulfate biosynthesis.The Journal of biological chemistry · 2026Article
- Biosynthesis and Regulation of Laminin-Binding O-Mannosyl Glycans Related to Muscular Dystrophy.Advances in experimental medicine and biology · 2026Review
- Article
- Genome-wide analyses reveal intricate genetic mechanisms underlying egg production efficiency in chickens.Journal of animal science and biotechnology · 2025Article
- Regulation of intracellular activity of N-glycan branching enzymes in mammals.The Journal of biological chemistry · 2024Review
- Protein O-mannosylation: one sugar, several pathways, many functions.Glycobiology · 2023Review
- Astrocytes: Lessons Learned from the Cuprizone Model.International journal of molecular sciences · 2023Review
- Glycosylation and behavioral symptoms in neurological disorders.Translational psychiatry · 2023Review
- Role of Fibrinogen in Type-2 Diabetes Mellitus with Diabetic Neuropathy and its Preliminary Mechanism.Protein and peptide letters · 2023Article
- Structure-based design of UDP-GlcNAc analogs as candidate GnT-V inhibitors.Biochimica et biophysica acta. General subjects · 2022Article
- Protein Tyrosine Phosphatase Receptor Type Z in Central Nervous System Disease.International journal of molecular sciences · 2022Review
- Mammalian brain glycoproteins exhibit diminished glycan complexity compared to other tissues.Nature communications · 2022Article
- Extracellular Vesicles and Glycosylation.Advances in experimental medicine and biology · 2021Article
- Investigation of neuro-inflammatory parameters in a cuprizone induced mouse model of multiple sclerosis.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
- Establishing Rules for Self-Adhesion and Aggregation ofLangmuir : the ACS journal of surfaces and colloids · 2020Article
- P2x7 receptors control demyelination and inflammation in the cuprizone model.Brain, behavior, & immunity - health · 2020Article
- 3D Structure and Function of Glycosyltransferases Involved inInternational journal of molecular sciences · 2020Review
- Mammalian O-mannosyl glycans: Biochemistry and glycopathology.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2019Article
- Recent advancements in understanding mammalian O-mannosylation.Glycobiology · 2017Review
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11 authors.
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Abstract
In demyelinating diseases such as multiple sclerosis, a critical problem is failure of remyelination, which is important for protecting axons against degeneration and restoring conduction deficits. However, the underlying mechanism of demyelination/remyelination remains unclear. N-acetylglucosaminyltransferase-IX (GnT-IX; also known as GnT-Vb) is a brain-specific glycosyltransferase that catalyzes the branched formation of O-mannosyl glycan structures. O-Mannosylation of α-dystroglycan is critical for its function as an extracellular matrix receptor, but the biological significance of its branched structures, which are exclusively found in the brain, is unclear. In this study, we found that GnT-IX formed branched O-mannosyl glycans on receptor protein tyrosine phosphatase β (RPTPβ) in vivo. Since RPTPβ is thought to play a regulatory role in demyelinating diseases, GnT-IX-deficient mice were subjected to cuprizone-induced demyelination. Cuprizone feeding for 8 weeks gradually promoted demyelination in wild-type mice. In GnT-IX-deficient mice, the myelin content in the corpus callosum was reduced after 4 weeks of treatment, but markedly increased at 8 weeks, suggesting enhanced remyelination under GnT-IX deficiency. Furthermore, astrocyte activation in the corpus callosum of GnT-IX-deficient mice was significantly attenuated, and an oligodendrocyte cell lineage analysis indicated that more oligodendrocyte precursor cells differentiated into mature oligodendrocytes. Together, branched O-mannosyl glycans in the corpus callosum in the brain are a necessary component of remyelination inhibition in the cuprizone-induced demyelination model, suggesting that modulation of O-mannosyl glycans is a likely candidate for therapeutic strategies.
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