ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Tenascin-R is an intrinsic autocrine factor for oligodendrocyte differentiation and promotes cell adhesion by a sulfatide-mediated mechanism.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 109 citations in OpenAlex.
- Oligodendrocyte Piezo2 is a regulator of age-dependent myelin integrity and dysregulated in multiple sclerosis.Communications biology · 2026Article
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- Developmental patterns of extracellular matrix molecules in the embryonic and postnatal mouse hindbrain.Frontiers in neuroanatomy · 2024Article
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- Nimodipine Exerts Beneficial Effects on the Rat Oligodendrocyte Cell Line OLN-93.Brain sciences · 2022Article
- Low-Dose Anti-HIV Drug Efavirenz Mitigates Retinal Vascular Lesions in a Mouse Model of Alzheimer's Disease.Frontiers in pharmacology · 2022Article
- The molecular regulation of oligodendrocyte development and CNS myelination by ECM proteins.Frontiers in cell and developmental biology · 2022Review
- Tenascins Interfere With Remyelination in an Ex Vivo Cerebellar Explant Model of Demyelination.Frontiers in cell and developmental biology · 2022Article
- Advancing models of neural development with biomaterials.Nature reviews. Neuroscience · 2021Review
- Adult-onset CNS myelin sulfatide deficiency is sufficient to cause Alzheimer's disease-like neuroinflammation and cognitive impairment.Molecular neurodegeneration · 2021Article
- The extracellular matrix as modifier of neuroinflammation and remyelination in multiple sclerosis.Brain : a journal of neurology · 2021Review
- Extracellular Matrix Remodeling in the Retina and Optic Nerve of a Novel Glaucoma Mouse Model.Biology · 2021Article
- Loss of Tenascin-X expression during tumor progression: A new pan-cancer marker.Matrix biology plus · 2020Article
- Early Days of Tenascin-R Research: Two Approaches Discovered and Shed Light on Tenascin-R.Frontiers in immunology · 2020Article
- The altered expression of perineuronal net elements during neural differentiation.Cellular & molecular biology letters · 2018Article
- Amyloid Proteins and Their Role in Multiple Sclerosis. Considerations in the Use of Amyloid-PET Imaging.Frontiers in neurology · 2016Review
- Transcriptional regulation of tenascin genes.Cell adhesion & migration · 2015Review
- Extracellular matrix regulation of inflammation in the healthy and injured spinal cord.Experimental neurology · 2014Review
- Role of sulfatide in normal and pathological cells and tissues.Journal of lipid research · 2012Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
O4(+) oligodendrocyte (OL) progenitors in the mammalian CNS are committed fully to terminal differentiation into myelin-forming cells. In the absence of other cell types in vitro, OL differentiation reproduces the in vivo development with a correct timing, suggesting the existence of an intrinsic regulatory mechanism that presently is unknown. We have examined the effect of two isoforms of the extracellular matrix (ECM) molecule tenascin-R (TN-R), which is expressed by OLs during the process of myelination, on the adhesion and maturation of OLs in vitro. Here we show that the substrate-bound molecules supported the adhesion of O4(+) OLs independently of the CNS region or age from which they were derived. At the molecular level this process was mediated by protein binding to membrane surface sulfatides (Sulf), as indicated by the interference of O4 antibody and Sulf with the attachment of OLs or other Sulf+ cells, erythrocytes, to TN-R substrates and by direct protein-glycolipid binding studies. In the absence of platelet-derived growth factor (PDGF), exogenous TN-R induced myelin gene expression and the upregulation of its own synthesis by cultured cells, resulting in a rapid terminal differentiation of O4(+) progenitors. Our findings strongly suggest that TN-R represents an intrinsic regulatory molecule that controls the timed OL differentiation by an autocrine mechanism and imply the relevance of TN-R for CNS myelination and remyelination.
Indexed as
Identifiers
9169525PMC6573339W1829681736What OpenQuestion holds
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.