ArticleJournal of neuroinflammation2011
Lipocalin 2 in the central nervous system host response to systemic lipopolysaccharide administration.
Article in Journal of neuroinflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 109 citations in OpenAlex.
- Trial
- DRP1 induces neuroinflammation via transcriptional regulation of NF-ĸB.Nature communications · 2026Article
- Lcn2 deficiency leads to long-lasting social impairments independent of maternal immune activation.Journal of neuroinflammation · 2026Article
- Article
- Targeted rescue of synaptic plasticity improves cognitive decline in sepsis-associated encephalopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Lipocalin-2 drives neuropsychiatric and cutaneous disease in MRL/lpr mice.Frontiers in immunology · 2024Article
- Mild Oxidative Stress Induced by Sodium Arsenite Reduces Lipocalin-2 Expression Levels in Cortical Glial Cells.International journal of molecular sciences · 2023Article
- Lipocalin-2: a therapeutic target to overcome neurodegenerative diseases by regulating reactive astrogliosis.Experimental & molecular medicine · 2023Review
- Article
- Transient ischemic stroke triggers sustained damage of the choroid plexus blood-CSF barrier.Frontiers in cellular neuroscience · 2023Article
- Up-regulation of LCN2 in the anterior cingulate cortex contributes to neural injury-induced chronic pain.Frontiers in cellular neuroscience · 2023Article
- Activation of TNF Receptor 2 Improves Synaptic Plasticity and Enhances Amyloid-β Clearance in an Alzheimer's Disease Mouse Model with Humanized TNF Receptor 2.Journal of Alzheimer's disease : JAD · 2023Article
- Astroglial and oligodendroglial markers in the cuprizone animal model for de- and remyelination.Histochemistry and cell biology · 2022Article
- Desferrioxamine Ameliorates Lipopolysaccharide-Induced Lipocalin-2 Upregulation via Autophagy Activation in Primary Astrocytes.Molecular neurobiology · 2022Article
- The role of neutrophil gelatinase-associated lipocalin and iron homeostasis in object recognition impairment in aged sepsis-survivor rats.Scientific reports · 2022Article
- Lipocalin-2 and Cerebral Stroke.Frontiers in molecular neuroscience · 2022Review
- The role of lipocalin 2 in brain injury and recovery after ischemic and hemorrhagic stroke.Frontiers in molecular neuroscience · 2022Review
- Neuroinflammation Induced by Transgenic Expression of Lipocalin-2 in Astrocytes.Frontiers in cellular neuroscience · 2022Article
- Microglial Cannabinoid Type 1 Receptor Regulates Brain Inflammation in a Sex-Specific Manner.Cannabis and cannabinoid research · 2021Article
- Tonicity-responsive enhancer-binding protein promotes diabetic neuroinflammation and cognitive impairment via upregulation of lipocalin-2.Journal of neuroinflammation · 2021Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundLipocalin 2 (Lcn2) is a bacteriostatic factor that may also modulate cellular function, however, little is known concerning the expression or role of Lcn2 in CNS inflammation. Therefore, here we investigated the regulation and possible function of Lcn2 in the CNS following peripheral lipopolysaccharide (LPS) injection in mice.
methodsA murine model for systemic endotoxemia was used in this study. Wild type or Lcn2 KO mice (both genotypes C57BL/6 strain) were given either a single or dual, staggered intraperitoneal injections of purified E. coli LPS or vehicle alone. The brain was examined for the expression and location of Lcn2 mRNA and protein and various markers for neuroinflammation were analyzed.
resultsAlthough undetectable under physiological conditions, both Lcn2 mRNA and protein were induced to high levels in the brain after LPS injection. By contrast, RNA corresponding to the putative Lcn2 (termed 24p3R) receptor was present at high levels in the normal brain and remained unaltered by LPS injection. Differences between Lcn2 and 24p3R mRNA expression were found at the anatomic and cellular level. Endothelial cells, microglia and the choroid plexus but not neurons were identified as the main cellular sources for Lcn2 mRNA in the CNS. By contrast, 24p3R mRNA was detected in neurons and the choroid plexus only. Lcn2 protein was found to have a similar cellular localization as the corresponding RNA transcripts with the exception that subsets of neurons were also strongly positive. Various inflammatory, glial, and iron handling markers were analyzed and found to have similar alterations between WT and Lcn2 KO animals.
conclusions1) Lcn2 production is strongly induced in the CNS by systemic LPS injection, 2) in addition to Lcn2 production at key gateways of bacterial entry to the CNS, neurons may be a target for the actions of Lcn2, which is apparently taken up by these cells, and 3) the cellular functions of Lcn2 in the CNS remain enigmatic.
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