ArticlePloS one2013
Lipocalin-2 expressed in innate immune cells is an endogenous inhibitor of inflammation in murine nephrotoxic serum nephritis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- Iron Biology in Acute Kidney Injury: Catalytic Iron, Hepcidin-Ferroportin Axis, and NGAL-A Narrative Review.International journal of molecular sciences · 2026Review
- The role of serum Neutrophil Gelatinase-Associated Lipocalin (NGAL) in detecting acute kidney injury in preterm neonates exposed to nephrotoxic drugs.BMC pediatrics · 2025Observational
- The dimethyloxalylglycine-functionalized nanofibers forMaterials today. Bio · 2025Article
- Understanding How Minerals Contribute to Optimal Immune Function.Journal of immunology research · 2023Review
- Iron Reshapes the Gut Microbiome and Host Metabolism.Journal of lipid and atherosclerosis · 2021Review
- Lipocalin 2 mediates appetite suppression during pancreatic cancer cachexia.Nature communications · 2021Article
- Regulation of theInfection and immunity · 2021Article
- Agonism of Prostaglandin E2 Receptor 4 Ameliorates Tubulointerstitial Injury in Nephrotoxic Serum Nephritis in Mice.Journal of clinical medicine · 2021Article
- TAM-ing the CIA-Tumor-Associated Macrophages and Their Potential Role in Unintended Side Effects of Therapeutics for Cancer-Induced Anemia.Frontiers in oncology · 2021Article
- Loss of Function of von Hippel-Lindau Trigger Lipocalin 2-Dependent Inflammatory Responses in Cultured and Primary Renal Tubular Cells.Oxidative medicine and cellular longevity · 2021Article
- Macrophage-Derived Iron-Bound Lipocalin-2 Correlates with Renal Recovery Markers Following Sepsis-Induced Kidney Damage.International journal of molecular sciences · 2020Article
- Lipocalin-2 Exacerbates Lupus Nephritis by Promoting Th1 Cell Differentiation.Journal of the American Society of Nephrology : JASN · 2020Article
- Lipocalin-2 deficiency may predispose to the progression of spontaneous age-related adiposity in mice.Scientific reports · 2020Article
- Neutrophil Gelatinase-Associated Lipocalin Protects from ANCA-Induced GN by Inhibiting TJournal of the American Society of Nephrology : JASN · 2020Article
- The role of lipocalin-2 in age-related macular degeneration (AMD).Cellular and molecular life sciences : CMLS · 2020Review
- Article
- Functions and regulation of lipocalin-2 in gut-origin sepsis: a narrative review.Critical care (London, England) · 2019Review
- Hypoxia Induces Astrocyte-Derived Lipocalin-2 in Ischemic Stroke.International journal of molecular sciences · 2019Article
- Exploring macrophage cell therapy on Diabetic Kidney Disease.Journal of cellular and molecular medicine · 2019Article
- Perspectives in Lipocalin-2: Emerging Biomarker for Medical Diagnosis and Prognosis for Alzheimer's Disease.Clinical nutrition research · 2018Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipocalin-2 (Lcn-2) is involved in divergent processes such as acute kidney injury or bacterial host defence. Our study was designed to evaluate the functional role of Lcn-2 in nephrotoxic serum nephritis (NTS). Since Lcn-2 is expressed in tubular epithelial cells as well as in cells of innate immunity such as macrophages and polymorphonuclear neutrophils (PMN), we induced NTS in wild-type (WT), Lcn-2 knock-out (KO) mice and WT/Lcn-2 KO chimeras. Mice lacking Lcn-2 exhibited more glomerular damage with increased proteinuria and interstitial leukocyte accumulation compared to WT mice. Chimeras able to express Lcn-2 in macrophages and PMN but not in epithelial cells were found to develop NTS comparable to wild-type controls. In contrast, chimeras expressing Lcn-2 in tubular epithelial cells with no expression in innate immune cells developed increased NTS due to decreased concerted apoptosis but increased necrosis and formation of damage-associated molecular patterns (DAMPs) such as high-mobility group box 1 (HMGB-1) in the kidney. In vivo blockade of HMGB-1, a toll-like receptor (TLR)-2 agonist, significantly reduced inflammation and NTS in Lcn-2 knock-out mice. In parallel, TLR-2 signalling was found to drive Lcn-2 transcription in vitro. Taken together, Lcn-2 expressed in innate immune cells is protective in NTS by inducing concerted apoptosis and inhibiting the formation of HMGB-1 thereby limiting cytokine production via TLR-2 signalling. In parallel, TLR-2 dependent transcription of Lcn-2 is an endogenous inhibitor of inflammation in NTS.
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