ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Lipocalin-2 is an autocrine mediator of reactive astrocytosis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers.
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Who cites it
153 citing papers in PubMed, 275 citations in OpenAlex.
- Trial
- Antimicrobial proteins regulating neuroinflammation.Annals of medicine · 2026Review
- Review
- Hippocampal Lipocalin-2 in T2DM Associated Neurodegeneration: A Therapeutic Perspective.Neurochemical research · 2026Review
- Nitric Oxide-S-Nitrosylation and Its Role in Neuroinflammation Associated with Neuropsychiatric Conditions.International journal of molecular sciences · 2026Review
- Improved efficiency of protein aggregate removal using ubiquitin with a signal peptide.BMB reports · 2026Article
- Lcn2 deficiency leads to long-lasting social impairments independent of maternal immune activation.Journal of neuroinflammation · 2026Article
- Obesity Aggravates Status Epilepticus Through Lipocalin-2-mediated Inflammation and Necroptosis.Neurochemical research · 2026Article
- Targeting lipocalin-2 for multiple sclerosis: a dual role in diagnosis and therapy.Frontiers in immunology · 2026Review
- Article
- Regulation of LCN-2/PI3K/Akt on TNF-α induced inflammatory response of porcine intramuscular adipocytes.In vitro cellular & developmental biology. Animal · 2025Article
- Review
- GPR37L1 identifies spinal cord astrocytes and protects neuropathic pain after nerve injury.Neuron · 2025Article
- Astrocytes in the mouse brain respond bilaterally to unilateral retinal neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The pathophysiological significance between autosomal dominant polycystic kidney disease and neutrophil gelatinase-associated lipocalin.Kidney research and clinical practice · 2025Article
- Generation and Characterization of Human iPSC-Derived Astrocytes with Potential for Modeling X-Linked Adrenoleukodystrophy Phenotypes.International journal of molecular sciences · 2025Article
- The role of age-related genes in idiopathic pulmonary fibrosis and molecular docking analysis of their drug targets.Frontiers in immunology · 2025Article
- Identification and Evaluation of Lipocalin-2 in Sepsis-Associated Encephalopathy via Machine Learning Approaches.Journal of inflammation research · 2025Article
- Article
- Role of lipocalin-2 in amyotrophic lateral sclerosis.Frontiers in aging neuroscience · 2025Review
93 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astrocytes, the most abundant glial cell type in the brain, provide metabolic and trophic support to neurons and modulate synaptic activity. In response to a brain injury, astrocytes proliferate and become hypertrophic with an increased expression of intermediate filament proteins. This process is collectively referred to as reactive astrocytosis. Lipocalin 2 (lcn2) is a member of the lipocalin family that binds to small hydrophobic molecules. We propose that lcn2 is an autocrine mediator of reactive astrocytosis based on the multiple roles of lcn2 in the regulation of cell death, morphology, and migration of astrocytes. lcn2 expression and secretion increased after inflammatory stimulation in cultured astrocytes. Forced expression of lcn2 or treatment with LCN2 protein increased the sensitivity of astrocytes to cytotoxic stimuli. Iron and BIM (Bcl-2-interacting mediator of cell death) proteins were involved in the cytotoxic sensitization process. LCN2 protein induced upregulation of glial fibrillary acidic protein (GFAP), cell migration, and morphological changes similar to characteristic phenotypic changes termed reactive astrocytosis. The lcn2-induced phenotypic changes of astrocytes occurred through a Rho-ROCK (Rho kinase)-GFAP pathway, which was positively regulated by nitric oxide and cGMP. In zebrafishes, forced expression of rat lcn2 gene increased the number and thickness of cellular processes in GFAP-expressing radial glia cells, suggesting that lcn2 expression in glia cells plays an important role in vivo. Our results suggest that lcn2 acts in an autocrine manner to induce cell death sensitization and morphological changes in astrocytes under inflammatory conditions and that these phenotypic changes may be the basis of reactive astrocytosis in vivo.
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Registered trials
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.