ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Targeted GAS6 delivery to the CNS protects axons from damage during experimental autoimmune encephalomyelitis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 80 citations in OpenAlex.
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- GAS6 as a potential target to alleviate neuroinflammation during Japanese encephalitis in mouse models.Journal of neuroinflammation · 2024Article
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- Microglial phagocytosis of single dying oligodendrocytes is mediated by CX3CR1 but not MERTK.Cell reports · 2024Article
- Administration of Gas6 attenuates lung fibrosis via inhibition of the epithelial-mesenchymal transition and fibroblast activation.Cell biology and toxicology · 2024Article
- HLA-DRB1*15:01 and theNeurology(R) neuroimmunology & neuroinflammation · 2024Article
- Growth arrest specific protein 6 alleviated white matter injury after experimental ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Gas6/TAM system as potential biomarker for multiple sclerosis prognosis.Frontiers in immunology · 2024Article
- Dietary vitamin K intake is associated with decreased neurofilament light chain among middle-aged and older adults from the NHANES.Frontiers in nutrition · 2024Article
- Microglial phagocytosis of single dying oligodendrocytes is mediated by CX3CR1 but not MERTK.bioRxiv : the preprint server for biology · 2023Article
- Gas6 Promotes Microglia Efferocytosis and Suppresses Inflammation Through Activating Axl/Rac1 Signaling in Subarachnoid Hemorrhage Mice.Translational stroke research · 2023Article
- Mertk-expressing microglia influence oligodendrogenesis and myelin modelling in the CNS.Journal of neuroinflammation · 2023Article
- Article
- Distinctive waves of innate immune response in the retina in experimental autoimmune encephalomyelitis.JCI insight · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Growth arrest-specific protein 6 (GAS6) is a soluble agonist of the TYRO3, AXL, MERTK (TAM) family of receptor tyrosine kinases identified to have anti-inflammatory, neuroprotective, and promyelinating properties. During experimental autoimmune encephalomyelitis (EAE), wild-type (WT) mice demonstrate a significant induction of Gas6, Axl, and Mertk but not Pros1 or Tyro3 mRNA. We tested the hypothesis that intracerebroventricular delivery of GAS6 directly into the CNS of WT mice during myelin oligodendrocyte glycoprotein (MOG)-induced EAE would improve the clinical course of disease relative to artificial CSF (ACSF)-treated mice. GAS6 did not delay disease onset, but significantly reduced the clinical scores during peak and chronic EAE. Mice receiving GAS6 for 28 d had preserved SMI31(+) neurofilament immunoreactivity, significantly fewer SMI32(+) axonal swellings and spheroids and less demyelination relative to ACSF-treated mice. Alternate-day subcutaneous IFNβ injection did not enhance GAS6 treatment effectiveness. Gas6(-/-) mice sensitized with MOG35-55 peptide exhibit higher clinical scores during late peak to early chronic disease, with significantly increased SMI32(+) axonal swellings and Iba1(+) microglia/macrophages, enhanced expression of several proinflammatory mRNA molecules, and decreased expression of early oligodendrocyte maturation markers relative to WT mouse spinal cords with scores for 8 consecutive days. During acute EAE, flow cytometry showed significantly more macrophages but not T-cell infiltrates in Gas6(-/-) spinal cords than WT spinal cords. Our data are consistent with GAS6 being protective during EAE by dampening the inflammatory response, thereby preserving axonal integrity and myelination.
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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.