ArticleCNS neuroscience & therapeutics2019
White matter T2 hyperintensities and blood-brain barrier disruption in the hyperacute stage of subarachnoid hemorrhage in male mice: The role of lipocalin-2.
Article in CNS neuroscience & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Lcn2 Promotes Ferroptosis in Intracerebral Hemorrhage by Targeting Keap1 Tyr572 and Restricting Nrf2 Activation.MedComm · 2026Article
- Therapeutic Potential of NLRP3 Inhibitor MCC950 in Aging Mice Stroke Outcomes.Translational stroke research · 2026Article
- Article
- Single-Cell Transcriptomics Revealed White Matter Repair Following Subarachnoid Hemorrhage.Translational stroke research · 2025Article
- Atorvastatin Protects Against the Macrophage/Microglia-Related Neuroinflammation via Inhibiting Lipocalin-2 in Mouse Experimental Intracerebral Hemorrhage Model.Cellular and molecular neurobiology · 2025Article
- Identification of pivotal genes and regulatory networks associated with SAH based on multi-omics analysis and machine learning.Scientific reports · 2025Article
- Inhibition of GPR17/ID2 Axis Improve Remyelination and Cognitive Recovery after SAH by Mediating OPC Differentiation in Rat Model.Translational stroke research · 2025Article
- Mechanisms and potential therapeutic molecular targets in blood-brain barrier disruption following subarachnoid hemorrhage: a review of early brain injury.Frontiers in neurology · 2025Review
- The mechanisms of white matter injury and immune system crosstalk in promoting the progression of Parkinson's disease: a narrative review.Frontiers in aging neuroscience · 2024Review
- Lipocalin 2 in the Paraventricular Thalamic Nucleus Contributes to DSS-Induced Depressive-Like Behaviors.Neuroscience bulletin · 2023Article
- Lipocalin-2-mediated astrocyte pyroptosis promotes neuroinflammatory injury via NLRP3 inflammasome activation in cerebral ischemia/reperfusion injury.Journal of neuroinflammation · 2023Article
- White Matter Injury: An Emerging Potential Target for Treatment after Subarachnoid Hemorrhage.Oxidative medicine and cellular longevity · 2023Review
- Myelin sheath injury and repairment after subarachnoid hemorrhage.Frontiers in pharmacology · 2023Review
- Iron homeostasis and post-hemorrhagic hydrocephalus: a review.Frontiers in neurology · 2023Review
- A timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2022Article
- Human ESC-derived immunity- and matrix- regulatory cells ameliorated white matter damage and vascular cognitive impairment in rats subjected to chronic cerebral hypoperfusion.Cell proliferation · 2022Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Astrocytic phagocytosis contributes to demyelination after focal cortical ischemia in mice.Nature communications · 2022Article
- The role of lipocalin 2 in brain injury and recovery after ischemic and hemorrhagic stroke.Frontiers in molecular neuroscience · 2022Review
- Lipocalin-2 and Cerebral Stroke.Frontiers in molecular neuroscience · 2022Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
aimsThe current study examined whether white matter injury occurs in the hyperacute (4 hours) phase after subarachnoid hemorrhage (SAH) and the potential role of blood-brain barrier (BBB) disruption and an acute phase protein, lipocalin 2 (LCN2), in that injury.
methodsSubarachnoid hemorrhage was induced by endovascular perforation in adult mice. First, wild-type (WT) mice underwent MRI 4 hours after SAH to detect white matter T2 hyperintensities. Second, changes in LCN2 expression and BBB disruption associated with the MRI findings were examined. Third, SAH-induced white matter injury at 4 hours was compared in WT and LCN2 knockout (LCN2 KO) mice.
resultsAt 4 hours, most animals had uni- or bilateral white matter T2 hyperintensities after SAH in WT mice that were associated with BBB disruption and LCN2 upregulation. However, some disruption and LCN2 upregulation was also found in mice with no T2-hyperintensity lesion. In contrast, there were no white matter T2 hyperintensities in LCN2 KO mice after SAH. LCN2 deficiency also attenuated BBB disruption, myelin damage, and oligodendrocyte loss.
conclusionsSubarachnoid hemorrhage causes very early BBB disruption and LCN2 expression in white matter that is associated with and may precede T2 hyperintensities. LCN2 deletion attenuates MRI changes and pathological changes in white matter after SAH.
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