ArticleCNS neuroscience & therapeutics2022
A timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage.
Article in CNS neuroscience & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Microglia-Derived Exosomal miR-223-3p Targets the RhoB-NF-κB-CCL11 Axis in Astrocytes and Relieves Neuronal Damage in Subarachnoid Hemorrhage.Neurochemical research · 2025Article
- Single-Cell Transcriptomics Revealed White Matter Repair Following Subarachnoid Hemorrhage.Translational stroke research · 2025Article
- Optimization and evaluation of an experimental subarachnoid hemorrhage model in mice.Scientific reports · 2025Article
- TIMP-3 Alleviates White Matter Injury After Subarachnoid Hemorrhage in Mice by Promoting Oligodendrocyte Precursor Cell Maturation.Cellular and molecular neurobiology · 2024Article
- ASK1-K716R reduces neuroinflammation and white matter injury via preserving blood-brain barrier integrity after traumatic brain injury.Journal of neuroinflammation · 2023Article
- White Matter Injury: An Emerging Potential Target for Treatment after Subarachnoid Hemorrhage.Oxidative medicine and cellular longevity · 2023Review
- Lipocalin-2-Mediated Insufficient Oligodendrocyte Progenitor Cell Remyelination for White Matter Injury After Subarachnoid Hemorrhage via SCL22A17 Receptor/Early Growth Response Protein 1 Signaling.Neuroscience bulletin · 2022Article
- A timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2022Article
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7 authors at 2 institutions in 2 countries.
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Abstract
aimsWhite matter (WM) injury is a critical factor associated with worse outcomes following subarachnoid hemorrhage (SAH). However, the detailed pathological changes are not completely understood. This study investigates temporal changes in the corpus callosum (CC), including WM edema and oligodendrocyte death after SAH, and the role of lipocalin-2 (LCN2) in those changes.
methodsSubarachnoid hemorrhage was induced in adult wild-type or LCN2 knockout mice via endovascular perforation. Magnetic resonance imaging was performed 4 hours, 1 day, and 8 days after SAH, and T2 hyperintensity changes within the CC were quantified to represent WM edema. Immunofluorescence staining was performed to evaluate oligodendrocyte death and proliferation.
resultsSubarachnoid hemorrhage induced significant CC T2 hyperintensity at 4 hours and 1 day that diminished significantly by 8 days post-procedure. Comparing changes between the 4 hours and 1 day, each individual mouse had an increase in CC T2 hyperintensity volume. Oligodendrocyte death was observed at 4 hours, 1 day, and 8 days after SAH induction, and there was progressive loss of mature oligodendrocytes, while immature oligodendrocytes/oligodendrocyte precursor cells (OPCs) proliferated back to baseline by Day 8 after SAH. Moreover, LCN2 knockout attenuated WM edema and oligodendrocyte death at 24 hours after SAH.
conclusionsSubarachnoid hemorrhage leads to T2 hyperintensity change within the CC, which indicates WM edema. Oligodendrocyte death was observed in the CC within 1 day of SAH, with a partial recovery by Day 8. SAH-induced WM injury was alleviated in an LCN2 knockout mouse model.
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