ArticleThe Journal of biological chemistry2014
Lipocalin-2 protein deficiency ameliorates experimental autoimmune encephalomyelitis: the pathogenic role of lipocalin-2 in the central nervous system and peripheral lymphoid tissues.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
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Who cites it
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.
- Association of Serum Lipocalin-2 Concentrations with Psoriasis and Psoriatic Arthritis: An Updated Meta-Analysis.Disease markers · 2019Pooled it
- Lipocalin-2 in Intracerebral Hemorrhage: Mechanisms, Biomarker Potential, and Therapeutic Targeting.Neuromolecular medicine · 2026Review
- Transcriptomic and functional annotation datasets for GV1001 peptide treatment in an experimental autoimmune encephalomyelitis mouse model.Data in brief · 2026Article
- Targeting lipocalin-2 for multiple sclerosis: a dual role in diagnosis and therapy.Frontiers in immunology · 2026Review
- Upregulation of lipocalin-2 in the retina of experimental autoimmune uveitis.The Journal of veterinary medical science · 2025Article
- The pathophysiological significance between autosomal dominant polycystic kidney disease and neutrophil gelatinase-associated lipocalin.Kidney research and clinical practice · 2025Article
- Alterations in neutrophil mRNA profiles in multiple sclerosis and identification of candidate genes for further investigation.Frontiers in neurology · 2025Article
- Ablation of lipocalin-2 reduces neuroinflammation in a mouse model of Krabbe disease.Scientific reports · 2024Article
- Post-symptomatic administration of hMSCs exerts therapeutic effects in SCA2 mice.Stem cell research & therapy · 2024Article
- The relationship between inflammatory markers, clinical characteristics, and cognitive performance in drug-naïve patients with schizophrenia.European archives of psychiatry and clinical neuroscience · 2024Article
- Aberrant activation of hippocampal astrocytes causes neuroinflammation and cognitive decline in mice.PLoS biology · 2024Article
- CXCR2 perturbation promotesJournal of medical microbiology · 2024Article
- Star power: harnessing the reactive astrocyte response to promote remyelination in multiple sclerosis.Neural regeneration research · 2024Review
- Gandouling Regulates Ferroptosis and Improves Neuroinflammation in Wilson's Disease Through the LCN2/NLRP3 Signaling Pathway.Journal of inflammation research · 2024Article
- Lipocalin-2 promotes breast cancer brain metastasis by enhancing tumor invasion and modulating brain microenvironment.Frontiers in oncology · 2024Review
- Comparative transcriptomics analysis identifies crucial genes and pathways during goose spleen development.Frontiers in immunology · 2024Article
- Lipocalin-2: a therapeutic target to overcome neurodegenerative diseases by regulating reactive astrogliosis.Experimental & molecular medicine · 2023Review
- mRNA expression profile reveals differentially expressed genes in splenocytes of experimental autoimmune encephalomyelitis model.International journal of experimental pathology · 2023Article
- Lipocalin-2-mediated astrocyte pyroptosis promotes neuroinflammatory injury via NLRP3 inflammasome activation in cerebral ischemia/reperfusion injury.Journal of neuroinflammation · 2023Article
- Expression Analysis of Lipocalin 2 (LCN2) in Reproductive and Non-Reproductive Tissues ofInternational journal of molecular sciences · 2023Article
18 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipocalin-2 (LCN2) plays an important role in cellular processes as diverse as cell growth, migration/invasion, differentiation, and death/survival. Furthermore, recent studies indicate that LCN2 expression and secretion by glial cells are induced by inflammatory stimuli in the central nervous system. The present study was undertaken to examine the regulation of LCN2 expression in experimental autoimmune encephalomyelitis (EAE) and to determine the role of LCN2 in the disease process. LCN2 expression was found to be strongly increased in spinal cord and secondary lymphoid tissues after EAE induction. In spinal cords astrocytes and microglia were the major cell types expressing LCN2 and its receptor 24p3R, respectively, whereas in spleens, LCN2 and 24p3R were highly expressed in neutrophils and dendritic cells, respectively. Furthermore, disease severity, inflammatory infiltration, demyelination, glial activation, the expression of inflammatory mediators, and the proliferation of MOG-specific T cells were significantly attenuated in Lcn2-deficient mice as compared with wild-type animals. Myelin oligodendrocyte glycoprotein-specific T cells in culture exhibited an increased expression of Il17a, Ifng, Rorc, and Tbet after treatment with recombinant LCN2 protein. Moreover, LCN2-treated glial cells expressed higher levels of proinflammatory cytokines, chemokines, and MMP-9. Adoptive transfer and recombinant LCN2 protein injection experiments suggested that LCN2 expression in spinal cord and peripheral immune organs contributes to EAE development. Taken together, these results imply LCN2 is a critical mediator of autoimmune inflammation and disease development in EAE and suggest that LCN2 be regarded a potential therapeutic target in multiple sclerosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.