ArticleDisease models & mechanisms2017
Schwann cells are activated by ATP released from neurons in an
Article in Disease models & mechanisms, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- The node of Ranvier influences theiScience · 2024Article
- IgM anti-GM2 antibodies in patients with multifocal motor neuropathy target Schwann cells and are associated with early onset.Journal of neuroinflammation · 2024Article
- Increased Cerebrospinal Fluid Adenosine 5'-Triphosphate Levels in Patients with Guillain-Barré Syndrome and Chronic Inflammatory Demyelinating Polyneuropathy.Neurology research international · 2024Article
- Clinical Features and Differences of Miller Fisher Syndrome in Southern China: Retrospective Analysis of 72 Patients in 13 Provinces of Southern China.Journal of clinical neurology (Seoul, Korea) · 2023Article
- Axolemmal nanoruptures arising from paranodal membrane injury induce secondary axon degeneration in murine Guillain-Barré syndrome.Journal of the peripheral nervous system : JPNS · 2023Article
- Review
- Models and methods to study Schwann cells.Journal of anatomy · 2022Review
- Latrotoxin-Induced Neuromuscular Junction Degeneration Reveals Urocortin 2 as a Critical Contributor to Motor Axon Terminal Regeneration.International journal of molecular sciences · 2022Article
- Neuronal activity-dependent ATP enhances the pro-growth effect of repair Schwann cell extracellular vesicles by increasing their miRNA-21 loading.Frontiers in cellular neuroscience · 2022Article
- Review
- Physiology of gangliosides and the role of antiganglioside antibodies in human diseases.Cellular & molecular immunology · 2020Review
- An Agonist of the CXCR4 Receptor Strongly Promotes Regeneration of Degenerated Motor Axon Terminals.Cells · 2019Article
- HIV-1 gp120 Promotes Lysosomal Exocytosis in Human Schwann Cells.Frontiers in cellular neuroscience · 2019Article
- Purinergic Receptors in Neurological Diseases With Motor Symptoms: Targets for Therapy.Frontiers in pharmacology · 2018Review
- Moving forward with the neuromuscular junction.Journal of neurochemistry · 2017Review
- Neurodegenerative disease: models, mechanisms, and a new hope.Disease models & mechanisms · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neuromuscular junction is exposed to different types of insult, including mechanical trauma, toxins and autoimmune antibodies and, accordingly, has retained through evolution a remarkable ability to regenerate. Regeneration is driven by multiple signals that are exchanged among the cellular components of the junction. These signals are largely unknown. Miller Fisher syndrome is a variant of Guillain-Barré syndrome caused by autoimmune antibodies specific for epitopes of peripheral axon terminals. Using an animal model of Miller Fisher syndrome, we recently reported that a monoclonal anti-polysialoganglioside GQ1b antibody plus complement damages nerve terminals with production of mitochondrial hydrogen peroxide, which activates Schwann cells. Several additional signaling molecules are likely to be involved in the activation of the regeneration program in these cells. Using an
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.