ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
NG2 is a major chondroitin sulfate proteoglycan produced after spinal cord injury and is expressed by macrophages and oligodendrocyte progenitors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
192 citing papers in PubMed, 476 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
- From origins to nomenclature: illuminating the landscape of CNS fibroblasts and fibroblast-like cells.Acta neuropathologica communications · 2026Review
- Loss of function of Noggin inhibits glial scar formation and motor function recovery after spinal cord injury.Frontiers in neural circuits · 2026Article
- Antigliotic guiding regenerative gel: a bioactive hydrogel platform for peripheral nerve and spinal cord repair.Frontiers in surgery · 2026Review
- In vivo programming of adult pericytes aids axon regeneration by providing cellular bridges for SCI repair.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Translational Relevance of Secondary Intracellular Signaling Cascades Following Traumatic Spinal Cord Injury.International journal of molecular sciences · 2024Review
- Nerve-Glial antigen 2: unmasking the enigmatic cellular identity in the central nervous system.Frontiers in immunology · 2024Review
- Axonal growth inhibitors and their receptors in spinal cord injury: from biology to clinical translation.Neural regeneration research · 2023Review
- Optogenetic spinal stimulation promotes new axonal growth and skilled forelimb recovery in rats with sub-chronic cervical spinal cord injury.Journal of neural engineering · 2023Article
- Article
- Reviving the use of inhibitors of matrix metalloproteases in spinal cord injury: a case for specificity.Neural regeneration research · 2023Article
- Understanding the Role of the Glial Scar through the Depletion of Glial Cells after Spinal Cord Injury.Cells · 2023Review
- Regulation of axonal regeneration after mammalian spinal cord injury.Nature reviews. Molecular cell biology · 2023Review
- Pathology-induced NG2 proteoglycan expression in microglia.Neural regeneration research · 2023Article
- USP1/UAF1-Stabilized METTL3 Promotes Reactive Astrogliosis and Improves Functional Recovery after Spinal Cord Injury through mThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- AAV Vector Mediated Delivery of NG2 Function Neutralizing Antibody and Neurotrophin NT-3 Improves Synaptic Transmission, Locomotion, and Urinary Tract Function after Spinal Cord Contusion Injury in Adult Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Tackling the glial scar in spinal cord regeneration: new discoveries and future directions.Frontiers in cellular neuroscience · 2023Review
- The mechanism of chemokine receptor ACKR2 in cognitive impairment in young rats with traumatic brain injury.American journal of translational research · 2023Article
- Exogenous FGF-1 Differently Regulates Oligodendrocyte Replenishment in an SCI Repair Model and Cultured Cells.Biomedicines · 2022Article
- The Notch Signaling Pathway Regulates Differentiation of NG2 Cells into Oligodendrocytes in Demyelinating Diseases.Cellular and molecular neurobiology · 2022Review
132 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Several extracellular matrix (ECM) molecules have been identified as potent inhibitors of neurite outgrowth in vitro and are believed to limit axonal growth after CNS injury. Recent studies have shown that different members of the chondroitin sulfate proteoglycan (CSPG) class of putatively inhibitory ECM molecules are expressed after a number of CNS injuries. The purpose of this study was to evaluate the relative amounts of individual CSPGs expressed after spinal cord injury (SCI) and identify their cells of origin. Evaluation of total soluble CSPGs 2 weeks after dorsal column lesion in the rat demonstrated that NG2 is highly upregulated and is a major CSPG species. Immunocytochemical analysis further demonstrated that NG2 expression is upregulated within 24 hr of injury, peaks at 1 week, and remains elevated for at least an additional 7 weeks. NG2 expression results from a multicellular response to injury, including both reactive macrophages and oligodendrocyte progenitors; astrocytes were not identified as a major source of NG2. Immunocytochemical analysis of other CSPG family members 7 d after injury showed moderate upregulation of versican, brevican, and neurocan, and downregulation of phosphacan. Axonal tracing experiments demonstrated dense NG2 labeling adjacent to the forward processes of transected corticospinal tract axons in a spatial profile that could restrict axonal growth. Thus, NG2 is a major component of this putatively inhibitory class of ECM molecules expressed at sites of SCI and may restrict axonal regeneration.
Indexed as
Identifiers
11923444PMC6758310W2097465856What 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.