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A timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage
dc.contributor.authorPeng, Kang
dc.contributor.authorKoduri, Sravanthi
dc.contributor.authorYe, Fenghui
dc.contributor.authorYang, Jinting
dc.contributor.authorKeep, Richard F.
dc.contributor.authorXi, Guohua
dc.contributor.authorHua, Ya
dc.date.accessioned2022-05-06T17:26:31Z
dc.date.available2023-07-06 13:26:30en
dc.date.available2022-05-06T17:26:31Z
dc.date.issued2022-06
dc.identifier.citationPeng, Kang; Koduri, Sravanthi; Ye, Fenghui; Yang, Jinting; Keep, Richard F.; Xi, Guohua; Hua, Ya (2022). "A timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage." CNS Neuroscience & Therapeutics (6): 842-850.
dc.identifier.issn1755-5930
dc.identifier.issn1755-5949
dc.identifier.urihttps://hdl.handle.net/2027.42/172271
dc.description.abstractAimsWhite 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.Lipocalin-2 deficiency attenuates corpus callosum T2 hyperintensity and oligodendrocyte death after SAH induction.
dc.publisherWiley Periodicals, Inc.
dc.subject.otherT2 hyperintensity
dc.subject.othercorpus callosum
dc.subject.otherlipocalin-2
dc.subject.otheroligodendrocytes
dc.subject.othersubarachnoid hemorrhage
dc.titleA timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage
dc.typeArticle
dc.rights.robotsIndexNoFollow
dc.subject.hlbsecondlevelNeurology and Neurosciences
dc.subject.hlbtoplevelHealth Sciences
dc.description.peerreviewedPeer Reviewed
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/172271/1/cns13812.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/172271/2/cns13812_am.pdf
dc.identifier.doi10.1111/cns.13812
dc.identifier.sourceCNS Neuroscience & Therapeutics
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dc.working.doiNOen
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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