Oligodendroglia Are Particularly Vulnerable to Oxidative Damage After Neurotrauma In Vivo

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 oligodendr...

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Bibliographic Details
Published in:Journal of experimental neuroscience 2018, Vol.12, p.1179069518810004-1179069518810004
Main Authors: Giacci, Marcus, Fitzgerald, Melinda
Format: Article
Language:English
Subjects:
Apoptosis
Authorship
Cell fate
Degeneration
Deoxyribonucleic acid
DNA
DNA damage
Fate maps
Genotype & phenotype
Glial stem cells
Hybridization
Lipid peroxidation
mRNA
Myelin
Nitration
Oligodendrocytes
Optic nerve
Oxidation
Phenotypes
Progenitor cells
Spinal cord
Studies
Therapeutic applications
Trauma
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Summary: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.
ISSN:1179-0695
1179-0695
DOI:10.1177/1179069518810004