ArticleScientific reports2018
Grey matter OPCs are less mature and less sensitive to IFNγ than white matter OPCs: consequences for remyelination.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- The prevalence of obstructive sleep apnea-hypopnea syndrome in patients with multiple sclerosis: a systematic review and meta-analysis.Frontiers in neurology · 2024Pooled it
- Pathological extracellular matrix changes in decellularized normal appearing gray matter and subpial multiple sclerosis lesions.iScience · 2026Article
- Myelin Repair as a Neuroprotective Strategy for Multiple Sclerosis: From Bench to Bedside.Medicina (Kaunas, Lithuania) · 2026Review
- Enhanced myelination potential of human mature oligodendrocytes by TNF and IFNG combination.Journal of neuroinflammation · 2026Article
- The Effect of Tumor Necrosis Factor-α and Interleu-Kin-1β on the Restorative Properties of Human Oligodendrocyte Precursor Cells In Vitro.Bioengineering (Basel, Switzerland) · 2025Article
- Multiple sclerosis: what have we learned and can we still learn from electron microscopy.Cellular and molecular life sciences : CMLS · 2025Review
- Plasticity of Myelination.Advances in neurobiology · 2025Review
- Heterogeneity in oligodendrocyte precursor cell proliferation is dynamic and driven by passive bioelectrical properties.Cell reports · 2024Article
- Long-term in vivo three-photon imaging reveals region-specific differences in healthy and regenerative oligodendrogenesis.Nature neuroscience · 2024Article
- Star power: harnessing the reactive astrocyte response to promote remyelination in multiple sclerosis.Neural regeneration research · 2024Review
- Herpes Simplex Virus type 1 inhibits autophagy in glial cells but requires ATG5 for the success of viral replication.Frontiers in microbiology · 2024Article
- Nerve-Glial antigen 2: unmasking the enigmatic cellular identity in the central nervous system.Frontiers in immunology · 2024Review
- Long-termbioRxiv : the preprint server for biology · 2023Article
- Glial progenitor cells of the adult human white and grey matter are contextually distinct.Glia · 2023Article
- Article
- Neuroprotection and neuroregeneration: roles for the white matter.Neural regeneration research · 2022Review
- Transcriptomic architecture of nuclei in the marmoset CNS.Nature communications · 2022Article
- Mitochondria in Myelinating Oligodendrocytes: Slow and Out of Breath?Metabolites · 2021Review
- GDE2 expression in oligodendroglia regulates the pace of oligodendrocyte maturation.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Article
- Impairing committed cholesterol biosynthesis in white matter astrocytes, but not grey matter astrocytes, enhances in vitro myelination.Journal of neurochemistry · 2021Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a chronic inflammatory disease characterized by the formation of demyelinated lesions in the central nervous system. At later stages of the disease repair in the form of remyelination often fails, which leads to axonal degeneration and neurological disability. For the regeneration of myelin, oligodendrocyte progenitor cells (OPCs) have to migrate, proliferate and differentiate into remyelinating oligodendrocytes. Remyelination occurs faster and is more extensive in grey matter (GM) lesions than in white matter (WM) lesions. Here, we examined differences in neonatal OPCs from GM (gmOPCs) and WM (wmOPCs), both intrinsically and in response to environmental (injury) signals. We show that gmOPCs are less mature than wmOPCs, both on morphological and on gene-expression level. Additionally, gmOPCs proliferate more and differentiate slower than wmOPCs. When exposed to astrocyte-secreted signals wmOPC, but not gmOPC, migration decreases. In addition, wmOPCs are more sensitive to the detrimental effects of IFNγ treatment on proliferation, differentiation, and process arborisation, which is potentiated by TNFα. Our results demonstrate that OPCs from GM and WM differ both intrinsically and in response to their environment, which may contribute to the difference in remyelination efficiency between GM and WM MS lesions.
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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.