ArticleJournal of neuroinflammation2020
The glycosyltransferase EXTL2 promotes proteoglycan deposition and injurious neuroinflammation following demyelination.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Multi-ancestry genome-wide association study of asthma exacerbations.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2022Pooled it
- Article
- The Future of PET Imaging in Multiple Sclerosis: Characterisation of Individual White Matter Lesions.Journal of clinical medicine · 2025Review
- Bruton's tyrosine kinase-bearing B cells and microglia in neuromyelitis optica spectrum disorder.Journal of neuroinflammation · 2023Article
- Progression of cerebral white matter hyperintensities is related to leucocyte gene expression.Brain : a journal of neurology · 2022Article
- Targeting Fibronectin to Overcome Remyelination Failure in Multiple Sclerosis: The Need for Brain- and Lesion-Targeted Drug Delivery.International journal of molecular sciences · 2022Review
- Chondroitin sulfate proteoglycans prevent immune cell phenotypic conversion and inflammation resolution via TLR4 in rodent models of spinal cord injury.Nature communications · 2022Article
- Prioritization of risk genes in multiple sclerosis by a refined Bayesian framework followed by tissue-specificity and cell type feature assessment.BMC genomics · 2022Article
- New insights into glial scar formation after spinal cord injury.Cell and tissue research · 2022Review
- Physiology and Pathophysiology of Heparan Sulfate in Animal Models: Its Biosynthesis and Degradation.International journal of molecular sciences · 2022Review
- Growth Differentiation Factor 15 Regulates Oxidative Stress-Dependent Ferroptosis Post Spinal Cord Injury by Stabilizing the p62-Keap1-Nrf2 Signaling Pathway.Frontiers in aging neuroscience · 2022Article
- Overcoming the inhibitory microenvironment surrounding oligodendrocyte progenitor cells following experimental demyelination.Nature communications · 2021Article
- Combination of Hydroxychloroquine and Indapamide Attenuates Neurodegeneration in Models Relevant to Multiple Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Chondrodysplasias With Multiple Dislocations Caused by Defects in Glycosaminoglycan Synthesis.Frontiers in genetics · 2021Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChondroitin sulfate proteoglycans (CSPGs) are potent inhibitors of axonal regrowth and remyelination. More recently, they have also been highlighted as a modulator of macrophage infiltration into the central nervous system in experimental autoimmune encephalomyelitis, an inflammatory model of multiple sclerosis.
methodsWe interrogated results from single nucleotide polymorphisms (SNPs) lying in or close to genes regulating CSPG metabolism in the summary results from two publicly available systematic studies of multiple sclerosis (MS) genetics. A demyelinating injury model in the spinal cord of exostosin-like 2 deficient (EXTL2
resultsThe strongest evidence for genetic association was seen for SNPs mapping to the region containing the glycosyltransferase exostosin-like 2 (EXTL2), an enzyme that normally suppresses CSPG biosynthesis. Six of these SNPs showed genome-wide significant evidence for association in one of the studies with concordant and nominally significant effects in the second study. We then went on to show that a demyelinating injury to the spinal cord of EXTL2
conclusionsThese results emphasize CSPGs as a prominent modulator of neuroinflammation and they highlight CSPGs accumulating in lesions in promoting axonal injury.
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