ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2023
Lipocalin-2 Is a Key Regulator of Neuroinflammation in Secondary Traumatic and Ischemic Brain Injury.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- Antimicrobial proteins regulating neuroinflammation.Annals of medicine · 2026Review
- Peptidoglycan recognition proteins in the brain: Role in neuroinflammation and behavioral consequences.Histology and histopathology · 2026Review
- Notoginsenoside R1 Attenuates Oxidative Damage After Intracerebral Hemorrhage by Inhibiting LCN2 and Promoting HO-1 in Astrocytes.Brain sciences · 2026Article
- Characterization of an isogenicInfection and immunity · 2026Article
- Low-intensity transcranial ultrasound neuromodulation promotes neuronal regeneration: A new hope for noninvasive treatment of neurodegenerative diseases.Neural regeneration research · 2026Article
- Hippocampal Lipocalin-2 in T2DM Associated Neurodegeneration: A Therapeutic Perspective.Neurochemical research · 2026Review
- LCN2/SLC22A17 mediates the phagocytosis of GABAergic synapses by oligodendrocyte progenitor cells and contributes to cancer-induced pain and comorbid anxiety-like behaviors in mice.Acta neuropathologica communications · 2026Article
- GBA1 F213I mutation increases the expression of LCN2 promoting neurodegeneration.Cell death and differentiation · 2026Article
- NF-κB activation in astrocytes impairs wound healing after traumatic brain injury in male mice.Nature communications · 2026Article
- Lcn2 deficiency leads to long-lasting social impairments independent of maternal immune activation.Journal of neuroinflammation · 2026Article
- SHIV.D Infection Alters Production and Protein Composition of Myeloid-Derived Extracellular Vesicles.International journal of molecular sciences · 2026Article
- Multi-genomics data mining identified critical transcription factors and immune response pathways in traumatic optic nerve injury and retinal injury.Frontiers in ophthalmology · 2026Article
- Activation of silent synapses driven by emerging technologies: mechanisms, disease associations, and prospects for clinical translation.Frontiers in synaptic neuroscience · 2026Review
- Adriamycin nephropathy induces sensorineural hearing loss via blood-labyrinth barrier breakdown in BALB/c mice.Scientific reports · 2025Article
- Article
- Normal Ageing Impacts the Extent and Diversity of Neural Plasticity Induced in the Mouse Brain With Repetitive Transcranial Magnetic Stimulation.Aging cell · 2025Article
- Neutrophil Gelatinase-Associated Lipocalin: A Shared Early Biomarker of Remote Organ Dysfunction in Blast-Induced Extremity Trauma.International journal of molecular sciences · 2025Article
- Non-invasive light flickering reinstates visual plasticity in adult mice via lipocalin 2.BMC biology · 2025Article
- Endoplasmic Reticulum Stress Drives Neuroinflammation Through Lipocalin 2 Upregulation in Retinal Microglia After Optic Nerve Injury.Investigative ophthalmology & visual science · 2025Article
- Role of lipocalin-2 in amyotrophic lateral sclerosis.Frontiers in aging neuroscience · 2025Review
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Reactive glial cells are hallmarks of brain injury. However, whether these cells contribute to secondary inflammatory pathology and neurological deficits remains poorly understood. Lipocalin-2 (LCN2) has inflammatory and neurotoxic effects in various disease models; however, its pathogenic role in traumatic brain injury remains unknown. The aim of the present study was to investigate the expression of LCN2 and its role in neuroinflammation following brain injury. LCN2 expression was high in the mouse brain after controlled cortical impact (CCI) and photothrombotic stroke (PTS) injury. Brain levels of LCN2 mRNA and protein were also significantly higher in patients with chronic traumatic encephalopathy (CTE) than in normal subjects. RT-PCR and immunofluorescence analyses revealed that astrocytes were the major cellular source of LCN2 in the injured brain. Lcn2 deficiency or intracisternal injection of an LCN2 neutralizing antibody reduced CCI- and PTS-induced brain lesions, behavioral deficits, and neuroinflammation. Mechanistically, in cultured glial cells, recombinant LCN2 protein enhanced scratch injury-induced proinflammatory cytokine gene expression and inhibited Gdnf gene expression, whereas Lcn2 deficiency exerted opposite effects. Together, our results from CTE patients, rodent brain injury models, and cultured glial cells suggest that LCN2 mediates secondary damage response to traumatic and ischemic brain injury by promoting neuroinflammation and suppressing the expression of neurotropic factors.
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