Academic Journal
A timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage
| العنوان: | A timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage |
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| المؤلفون: | Peng, Kang, Koduri, Sravanthi, Ye, Fenghui, Yang, Jinting, Keep, Richard F., Xi, Guohua, Hua, Ya |
| المساهمون: | National Institute of Neurological Disorders and Stroke |
| المصدر: | CNS Neuroscience & Therapeutics ; volume 28, issue 6, page 842-850 ; ISSN 1755-5930 1755-5949 |
| بيانات النشر: | Wiley |
| سنة النشر: | 2022 |
| المجموعة: | Wiley Online Library (Open Access Articles via Crossref) |
| الوصف: | Aims White 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. Methods Subarachnoid 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. Results Subarachnoid 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. Conclusions Subarachnoid 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. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| DOI: | 10.1111/cns.13812 |
| الاتاحة: | http://dx.doi.org/10.1111/cns.13812 https://onlinelibrary.wiley.com/doi/pdf/10.1111/cns.13812 https://onlinelibrary.wiley.com/doi/full-xml/10.1111/cns.13812 |
| Rights: | http://creativecommons.org/licenses/by/4.0/ |
| رقم الانضمام: | edsbas.A612DB15 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1111/cns.13812 |
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