ArticleJournal of experimental neuroscience2018
Oligodendroglia Are Particularly Vulnerable to Oxidative Damage After Neurotrauma In Vivo.
Article in Journal of experimental neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed.
- Relationships betweenNeurology · 2019Trial
- Role of Oxidative Stress in the Occurrence and Development of Cognitive Dysfunction in Patients with Obstructive Sleep Apnea Syndrome.Molecular neurobiology · 2024Review
- Potential for a cerebellar role in moderate-late preterm associated behavioural disorders.Frontiers in pediatrics · 2024Review
- What Are the Roles of Oligodendrocyte Precursor Cells in Normal and Pathologic Conditions?Neurology · 2023Article
- Cell-specific alterations in autophagy-lysosomal activity near the chronically implanted microelectrodes.Biomaterials · 2023Article
- Secondary Degeneration Impairs Myelin Ultrastructural Development in Adulthood following Adolescent Neurotrauma in the Rat Optic Nerve.International journal of molecular sciences · 2023Article
- Dual isolation of primary neurons and oligodendrocytes from guinea pig frontal cortex.Frontiers in cellular neuroscience · 2023Article
- Review
- Brain organoids: A promising model to assess oxidative stress-induced central nervous system damage.Developmental neurobiology · 2021Review
- Oxidative stress and impaired oligodendrocyte precursor cell differentiation in neurological disorders.Cellular and molecular life sciences : CMLS · 2021Review
- Hemoglobin induces oxidative stress and mitochondrial dysfunction in oligodendrocyte progenitor cells.Translational research : the journal of laboratory and clinical medicine · 2021Article
- Is Oxidative Stress the Link Between Cerebral Small Vessel Disease, Sleep Disruption, and Oligodendrocyte Dysfunction in the Onset of Alzheimer's Disease?Frontiers in physiology · 2021Review
- When glia meet induced pluripotent stem cells (iPSCs).Molecular and cellular neurosciences · 2020Review
- Novel Treatment Strategies Targeting Myelin and Oligodendrocyte Dysfunction in Schizophrenia.Frontiers in psychiatry · 2020Review
- Strategies for Oligodendrocyte and Myelin Repair in Traumatic CNS Injury.Frontiers in cellular neuroscience · 2020Review
- Pre-clinical and Clinical Implications of "Inside-Out" vs. "Outside-In" Paradigms in Multiple Sclerosis Etiopathogenesis.Frontiers in cellular neuroscience · 2020Review
- The Influence of Reactive Oxygen Species in the Immune System and Pathogenesis of Multiple Sclerosis.Autoimmune diseases · 2020Review
- Review: immunoassays in DNA damage and instability detection.Cellular and molecular life sciences : CMLS · 2019Review
- An augmentation in histone dimethylation at lysine nine residues elicits vision impairment following traumatic brain injury.Free radical biology & medicine · 2019Article
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2 authors.
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No grant is acknowledged in the PubMed record.
Abstract
In the paper "Oligodendroglia are particularly vulnerable to oxidative damage after neurotrauma in vivo," we determined the extent of oxidative damage to specific cellular subpopulations and structures within regions vulnerable to secondary degeneration and assessed the effect this had on oligodendroglial function. Comparative assessment of oxidative damage demonstrated selective vulnerability of oligodendroglia, specifically oligodendrocyte progenitor cells (OPCs) to DNA oxidation in vivo. Immunohistochemical fate mapping along the oligodendroglial lineage showed a transient susceptibility of these cells to DNA oxidation, protein nitration, and lipid peroxidation, with mature oligodendrocytes derived immediately after injury more vulnerable to DNA oxidation than their counterparts existing at the time of injury or later derived. In situ hybridization demonstrated a reduction in myelin regulatory factor (MyRF) messenger RNA (mRNA) fluorescence in newly derived mature oligodendrocytes, suggesting a compromise in the production and maintenance of the myelin sheath in these cells. The data imply a deficit in the normal differentiation of OPCs to myelinating oligodendrocytes, associated with a transient increase in oxidative damage, which may contribute to the dysmyelinating phenotype seen at chronic time points after injury. Identifying and understanding the sources of this oxidative damage is integral for the development of therapeutic interventions for neurotrauma.
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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.