ArticleGlia2010
Effects of axon degeneration on oligodendrocyte lineage cells: dorsal rhizotomy evokes a repair response while axon degeneration rostral to spinal contusion induces both repair and apoptosis.
Article in Glia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- MiR499-5P loaded MSC derived exosomes affect oxidative stress and inflammatory response after spinal cord injury by targeting genes.Journal of orthopaedic surgery and research · 2025Article
- Neurodegeneration and inflammation crosstalk: Therapeutic targets and perspectives.IBRO neuroscience reports · 2023Article
- miR-6315 silencing protects against spinal cord injury through the Smo and anti-ferroptosis pathway.Bioscience reports · 2023Article
- Exogenous FGF-1 Differently Regulates Oligodendrocyte Replenishment in an SCI Repair Model and Cultured Cells.Biomedicines · 2022Article
- Electroacupuncture promotes the recovery of rats with spinal cord injury by suppressing the Notch signaling pathway via the H19/EZH2 axis.Annals of translational medicine · 2021Article
- Genome-wide analysis of acute traumatic spinal cord injury-related RNA expression profiles and uncovering of a regulatory axis in spinal fibrotic scars.Cell proliferation · 2021Article
- Acute brain inflammation, white matter oxidative stress, and myelin deficiency in a model of neonatal intraventricular hemorrhage.Journal of neurosurgery. Pediatrics · 2020Article
- Neonatal hydrocephalus leads to white matter neuroinflammation and injury in the corpus callosum of Ccdc39 hydrocephalic mice.Journal of neurosurgery. Pediatrics · 2020Article
- Delayed short-term tamoxifen treatment does not promote remyelination or neuron sparing after spinal cord injury.PloS one · 2020Article
- Review
- Editorial: Glia in Health and Disease.Frontiers in molecular neuroscience · 2019Article
- The Biology of Regeneration Failure and Success After Spinal Cord Injury.Physiological reviews · 2018Review
- The Involvement of the Myelin-Associated Inhibitors and Their Receptors in CNS Plasticity and Injury.Molecular neurobiology · 2018Review
- A novel inhibitor of p75-neurotrophin receptor improves functional outcomes in two models of traumatic brain injury.Brain : a journal of neurology · 2016Article
- Fluoxetine prevents oligodendrocyte cell death by inhibiting microglia activation after spinal cord injury.Journal of neurotrauma · 2015Article
- Electroacupuncture in the repair of spinal cord injury: inhibiting the Notch signaling pathway and promoting neural stem cell proliferation.Neural regeneration research · 2015Article
- Changes in NG2 cells and oligodendrocytes in a new model of intraspinal hemorrhage.Experimental neurology · 2014Article
- Review
- Safety of epicenter versus intact parenchyma as a transplantation site for human neural stem cells for spinal cord injury therapy.Stem cells translational medicine · 2013Article
- Gene expression profiling of liver X receptor α and Bcl-2-associated X protein in experimental transection spinal cord-injured rats.The journal of spinal cord medicine · 2013Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Wallerian degeneration in the dorsal columns (DC) after spinal cord injury (SCI) is associated with microglial activation and prolonged oligodendrocyte (OL) apoptosis that may contribute to demyelination and dysfunction after SCI. But, there is an increase in OL lineage cells after SCI that may represent a reparative response, and there is evidence for remyelination after SCI. To assess the role of axonal degeneration per se in OL apoptosis and proliferation, we cut the L2-S2 dorsal roots producing massive axonal degeneration and microglial activation in the DC, and found no evidence of OL loss or apoptosis. Rather, the numbers of OL-lineage cells positive for NG2 and APC (CC1) increased, and BrdU studies suggested new OL formation. We then tested contusion SCI (cSCI) that results in comparable degeneration in the DC rostral to the injury, microglial activation, and apoptosis of DC OLs by eight days. NG2+ cell proliferation and oligodendrogenesis was seen as after rhizotomy. The net result of this combination of proliferation and apoptosis was a reduction in DC OLs, confirming earlier studies. Using an antibody to oxidized nucleic acids, we found rapid and prolonged RNA oxidation in OLs rostral to cSCI, but no evidence of oxidative stress in DC OLs after rhizotomy. These results suggest that signals associated with axonal degeneration are sufficient to induce OL proliferation, and that secondary injury processes associated with the central SCI, including oxidative stress, rather than axonal degeneration per se, are responsible for OL apoptosis.
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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.