ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2014
Lipocalin-2 deficiency attenuates neuroinflammation and brain injury after transient middle cerebral artery occlusion in mice.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.
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Who cites it
98 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Integrated Analysis of Expression Profile Based on Differentially Expressed Genes in Middle Cerebral Artery Occlusion Animal Models.International journal of molecular sciences · 2016Pooled it
- Lcn2 Promotes Ferroptosis in Intracerebral Hemorrhage by Targeting Keap1 Tyr572 and Restricting Nrf2 Activation.MedComm · 2026Article
- Lipocalin-2 perpetuates postoperative and post-infectious neuroinflammation and anxiety-like behavior.Brain, behavior, and immunity · 2026Article
- Hippocampal Lipocalin-2 in T2DM Associated Neurodegeneration: A Therapeutic Perspective.Neurochemical research · 2026Review
- TIA1-mediated stress granules inhibit the neuroinflammation and neurodegeneration after spinal cord injury through LCN2 signaling.Cellular and molecular life sciences : CMLS · 2026Article
- Anti-Inflammatory and Antioxidant Effects of ω-3 Polyunsaturated Fatty Acids on Astrocytes and Their Implications for the Blood-Brain Barrier's Integrity and Function.International journal of molecular sciences · 2026Review
- Lipocalin-2 in Intracerebral Hemorrhage: Mechanisms, Biomarker Potential, and Therapeutic Targeting.Neuromolecular medicine · 2026Review
- Lcn2 deficiency leads to long-lasting social impairments independent of maternal immune activation.Journal of neuroinflammation · 2026Article
- Lipocalin 2: a double-edged sword in cellular ferroptosis.Cell biology and toxicology · 2026Review
- Obesity Aggravates Status Epilepticus Through Lipocalin-2-mediated Inflammation and Necroptosis.Neurochemical research · 2026Article
- Emerging roles of lipocalin-2-mediated neuroimmune interactions in chronic pain and itch.Frontiers in pharmacology · 2026Review
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- Hydroxysafflower yellow A alleviates the inflammatory response in astrocytes following cerebral ischemia by inhibiting the LCN2/STAT3 feedback loop.Metabolic brain disease · 2025Article
- Active Cryptococcus neoformans glucuronoxylomannan production prevents elimination of cryptococcal CNS infection in vivo.Journal of neuroinflammation · 2025Article
- Microglial cell proliferation is regulated, in part, by reactive astrocyte ETBExperimental neurology · 2025Article
- LCN2 induces neuronal loss and facilitates sepsis-associated cognitive impairments.Cell death & disease · 2025Article
- Lipocalin-2 in preoperative cerebrospinal fluid is a biomarker for postoperative delirium after hip fracture surgery in older adults: a prospective cohort study.Frontiers in neurology · 2025Article
- Platelet Membrane-Based Nanoparticles for Targeted Delivery of Deferoxamine to Alleviate Brain Injury Induced by Ischemic Stroke.International journal of nanomedicine · 2025Article
- Mechanism of LCN2 in cerebral ischemia-reperfusion injury.Frontiers in neuroscience · 2025Review
- Aberrant activation of hippocampal astrocytes causes neuroinflammation and cognitive decline in mice.PLoS biology · 2024Article
38 more citing papers are in PubMed but not listed here.
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9 authors.
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Abstract
Lipocalin-2 (LCN2) is a secreted protein of the lipocalin family, but little is known about the expression or the role of LCN2 in the central nervous system. Here, we investigated the role of LCN2 in ischemic stroke using a rodent model of transient cerebral ischemia. Lipocalin-2 expression was highly induced in the ischemic brain and peaked at 24 hours after reperfusion. After transient middle cerebral artery occlusion, LCN2 was predominantly expressed in astrocytes and endothelial cells, whereas its receptor (24p3R) was mainly detected in neurons, astrocytes, and endothelial cells. Brain infarct volumes, neurologic scores, blood-brain barrier (BBB) permeabilities, glial activation, and inflammatory mediator expression were significantly lower in LCN2-deficient mice than in wild-type animals. Lipocalin-2 deficiency also attenuated glial neurotoxicity in astrocyte/neuron cocultures after oxygen-glucose deprivation. Our results indicate LCN2 has a critical role in brain injury after ischemia/reperfusion, and that LCN2 may contribute to neuronal cell death in the ischemic brain by promoting neurotoxic glial activation, neuroinflammation, and BBB disruption.
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