ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Differential sulfation remodelling of heparan sulfate by extracellular 6-O-sulfatases regulates fibroblast growth factor-induced boundary formation by glial cells: implications for glial cell transplantation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- DNA Methylation Landscape of ReNcell Common Neural Progenitor Cell Lines Reveals Distinct Lineage Bias.Biology · 2026Article
- Heparan sulphate and neural development: dissecting the roles of astrocyte-expressed heparan sulphate.Biochemical Society transactions · 2025Review
- Supervised Machine-Based Learning and Computational Analysis to Reveal Unique Molecular Signatures Associated with Wound Healing and Fibrotic Outcomes to Lens Injury.International journal of molecular sciences · 2025Article
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- Importance of Heparan Sulfate Proteoglycans in Pancreatic Islets and β-Cells.International journal of molecular sciences · 2022Review
- Fibroblast Growth Factor Signalling in the Diseased Nervous System.Molecular neurobiology · 2021Review
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- Heparan Sulfate Synthesized byMolecular cancer research : MCR · 2021Article
- Multi-target approaches to CNS repair: olfactory mucosa-derived cells and heparan sulfates.Nature reviews. Neurology · 2020Review
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- Concise Review: The Endothelial Cell Extracellular Matrix Regulates Tissue Homeostasis and Repair.Stem cells translational medicine · 2019Review
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- Heparanase attenuates axon degeneration following sciatic nerve transection.Scientific reports · 2018Article
- A Unique TGFB1-Driven Genomic Program Links Astrocytosis, Low-Grade Inflammation and Partial Demyelination in Spinal Cord Periplaques from Progressive Multiple Sclerosis Patients.International journal of molecular sciences · 2017Article
- Epigenetic Regulation of the Biosynthesis & Enzymatic Modification of Heparan Sulfate Proteoglycans: Implications for Tumorigenesis and Cancer Biomarkers.International journal of molecular sciences · 2017Review
- Decreased Expression of Sulfatase 2 in the Brains of Alzheimer's Disease Patients: Implications for Regulation of Neuronal Cell Signaling.Journal of Alzheimer's disease reports · 2017Article
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- The role of heparan sulphate in development: the ectodermal story.International journal of experimental pathology · 2016Review
- Extracellular distribution of diffusible growth factors controlled by heparan sulfate proteoglycans during mammalian embryogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
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6 authors at 1 institution in 1 country.
Funding
Abstract
Previously, it has been shown that rat Schwann cells (SCs), but not olfactory ensheathing cells (OECs), form a boundary with astrocytes, due to a SC-specific secreted factor. Here, we identify highly sulfated heparan sulfates (HSs) and fibroblast growth factors (FGFs) 1 and 9 as possible determinants of boundary formation induced by rat SCs. Disaccharide analysis of HS in SC-conditioned and rat OEC-conditioned media showed that SCs secrete more highly sulfated HS than OECs. The dependence of the boundary-forming activity on high levels of sulfation was confirmed using a panel of semisynthetic modified heparins with variable levels of sulfation. Furthermore, extracellular HS 6-O-endosulfatase enzymes, Sulf 1 and Sulf 2, were expressed at a significantly lower level by SCs compared with OECs, and siRNA reduction of Sulfs in OECs was, in itself, sufficient to induce boundary formation. This demonstrates a key role for remodelling (reduction) of HS 6-O-sulfation by OECs, compared with SCs, to suppress boundary formation. Furthermore, specific anti-FGF1 and anti-FGF9 antibodies disrupted SC-astrocyte boundary formation, supporting a role for an HS sulfation-dependent FGF signaling mechanism via FGF receptors on astrocytes. We propose a model in which FGF1 and FGF9 signaling is differentially modulated by patterns of glial cell HS sulfation, dependent on Sulf 1 and Sulf 2 expression, to control FGF receptor 3-IIIb-mediated astrocytic responses. Moreover, these data suggest manipulation of HS sulfation after CNS injury as a potential novel approach for therapeutic intervention in CNS repair.
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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.