ArticleFrontiers in cellular neuroscience2022
Neu1 Is Released From Activated Microglia, Stimulating Microglial Phagocytosis and Sensitizing Neurons to Glutamate.
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- IgM Hyposialylation Modulates Podocyte Vulnerability in Patients With Idiopathic Nephrotic Syndrome.Kidney international reports · 2026Article
- Neu1 inhibition restrains BCoV replication and modulates ZBP1-dependent PANoptosis.Veterinary research · 2026Article
- Sialylation patterns in cerebral amyloid angiopathy.Brain pathology (Zurich, Switzerland) · 2026Article
- St6gal1-mediated sialylation protects retinal ganglion cells by restraining microglial phagocytosis.Journal of neuroinflammation · 2026Article
- Alterations in secondary lipids are associated with neuroinflammation in the brain of Neu1-deficient mice.Cell and tissue research · 2026Article
- Desialylation and sialidase secretion from monocytes and macrophages upon LPS activation.Frontiers in immunology · 2026Article
- Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026Review
- Epididymal epithelial cells facilitate NEU1 loading to modulate sperm α-2,6 sialylation, enhance maturation and motility.Cellular and molecular life sciences : CMLS · 2025Article
- Proteomic analysis of cerebrospinal fluid from females with multiple sclerosis highlights elevated microglial function and impaired neurogenesis.IBRO neuroscience reports · 2025Article
- Microglial replacement in a Sandhoff disease mouse model reveals myeloid-derived β-hexosaminidase is necessary for neuronal health.Nature communications · 2025Article
- NEU1-Mediated Extracellular Vesicle Glycosylation in Alzheimer's Disease: Mechanistic Insights into Intercellular Communication and Therapeutic Targeting.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Macrophages release neuraminidase and cleaved calreticulin for programmed cell removal.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Supporting Neurologic Health with Mushroom Nutrition.Nutrients · 2025Review
- Neuraminidase 1 regulates neuropathogenesis by governing the cellular state of microglia via modulation of Trem2 sialylation.Cell reports · 2025Article
- New use of an old drug: mechanism of oseltamivir phosphate inhibiting liver cancer through regulation of lipophagy via NEU1.Frontiers in pharmacology · 2025Article
- Myeloid-derived β-hexosaminidase is essential for neuronal health and lysosome function: implications for Sandhoff disease.bioRxiv : the preprint server for biology · 2024Article
- Neuraminidase-1 (NEU1): Biological Roles and Therapeutic Relevance in Human Disease.Current issues in molecular biology · 2024Review
- Proteomic Analysis to Identify Prospective Biomarkers of Treatment Outcome After Microvascular Decompression for Trigeminal Neuralgia: A Preliminary Study.The journal of pain · 2024Article
- Microglia Mediate Contact-Independent Neuronal Network Remodeling via Secreted Neuraminidase-3 Associated with Extracellular Vesicles.ACS central science · 2023Article
- Activated microglia release β-galactosidase that promotes inflammatory neurodegeneration.Frontiers in aging neuroscience · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neuraminidase 1 (Neu1) hydrolyses terminal sialic acid residues from glycoproteins and glycolipids, and is normally located in lysosomes, but can be released onto the surface of activated myeloid cells and microglia. We report that endotoxin/lipopolysaccharide-activated microglia released Neu1 into culture medium, and knockdown of Neu1 in microglia reduced both Neu1 protein and neuraminidase activity in the culture medium. Release of Neu1 was reduced by inhibitors of lysosomal exocytosis, and accompanied by other lysosomal proteins, including protective protein/cathepsin A, known to keep Neu1 active. Extracellular neuraminidase or over-expression of Neu1 increased microglial phagocytosis, while knockdown of Neu1 decreased phagocytosis. Microglial activation caused desialylation of microglial phagocytic receptors Trem2 and MerTK, and increased binding to Trem2 ligand galectin-3. Culture media from activated microglia contained Neu1, and when incubated with neurons induced their desialylation, and increased the neuronal death induced by low levels of glutamate. Direct desialylation of neurons by adding sialidase or inhibiting sialyltransferases also increased glutamate-induced neuronal death. We conclude that activated microglia can release active Neu1, possibly by lysosomal exocytosis, and this can both increase microglial phagocytosis and sensitize neurons to glutamate, thus potentiating neuronal death.
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