ArticleActa neuropathologica communications2020
Acute brain injuries trigger microglia as an additional source of the proteoglycan NG2.
Article in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- NG2 Glia and Cellular Crosstalk in Health and Disease: Focus on Spinal Cord Injury.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Structure and Function of Ocular Proteoglycans: Essential Proteins for Vision.International journal of molecular sciences · 2026Review
- From origins to nomenclature: illuminating the landscape of CNS fibroblasts and fibroblast-like cells.Acta neuropathologica communications · 2026Review
- Sex- and age- differences in the expression of critical blood-brain barrier regulators: a physiological context.Biology of sex differences · 2025Article
- Oligodendroglia and Myelin: Supporting the Connectome.Advances in neurobiology · 2025Review
- Genetic Downregulation of GABACells · 2024Article
- Article
- Inhibiting CaNature neuroscience · 2024Article
- A New Acquaintance of Oligodendrocyte Precursor Cells in the Central Nervous System.Neuroscience bulletin · 2024Review
- Adenosine triggers early astrocyte reactivity that provokes microglial responses and drives the pathogenesis of sepsis-associated encephalopathy in mice.Nature communications · 2024Article
- Effects of Moleac 901 after severe spinal cord injury on chronic phase in Wistar rats.Heliyon · 2024Article
- Glial cells react to closed head injury in a distinct and spatiotemporally orchestrated manner.Scientific reports · 2024Article
- Nerve-Glial antigen 2: unmasking the enigmatic cellular identity in the central nervous system.Frontiers in immunology · 2024Review
- Roles and regulation of microglia activity in multiple sclerosis: insights from animal models.Nature reviews. Neuroscience · 2023Review
- Review
- NF-κB is a critical mediator of post-mitotic senescence in oligodendrocytes and subsequent white matter loss.Molecular neurodegeneration · 2023Article
- Pathology-induced NG2 proteoglycan expression in microglia.Neural regeneration research · 2023Article
- Article
- The origins and dynamic changes of C3- and S100A10-positive reactive astrocytes after spinal cord injury.Frontiers in cellular neuroscience · 2023Article
- NG2-glia crosstalk with microglia in health and disease.CNS neuroscience & therapeutics · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NG2 is a type I transmembrane glycoprotein known as chondroitin sulfate proteoglycan 4 (CSPG4). In the healthy central nervous system, NG2 is exclusively expressed by oligodendrocyte progenitor cells and by vasculature pericytes. A large body of immunohistochemical studies showed that under pathological conditions such as acute brain injuries and experimental autoimmune encephalomyelitis (EAE), a number of activated microglia were NG2 immuno-positive, suggesting NG2 expression in these cells. Alternative explanations for the microglial NG2 labeling consider the biochemical properties of NG2 or the phagocytic activity of activated microglia. Reportedly, the transmembrane NG2 proteoglycan can be cleaved by a variety of proteases to deposit the NG2 ectodomain into the extracellular matrix. The ectodomain, however, could also stick to the microglial surface. Since microglia are phagocytic cells engulfing debris of dying cells, it is difficult to identify a genuine expression of NG2. Recent studies showing (1) pericytes giving rise to microglial after stroke, and (2) immune cells of NG2-EYFP knock-in mice lacking NG2 expression in an EAE model generated doubts for the de novo expression of NG2 in microglia after acute brain injuries. In the current study, we took advantage of three knock-in mouse lines (NG2-CreERT2, CX
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