ArticleScientific reports2016
Macrophage-derived Lipocalin-2 contributes to ischemic resistance mechanisms by protecting from renal injury.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Traditional Chinese Medicine and renal regeneration: experimental evidence and future perspectives.Chinese medicine · 2024Review
- NGAL in the Development of Acute Kidney Injury in a Murine Model of Remote Ischaemic Preconditioning and Liver Ischaemia Reperfusion.International journal of molecular sciences · 2024Article
- Ovaries of estrogen receptor 1-deficient mice show iron overload and signs of aging.Frontiers in endocrinology · 2024Article
- The von Hippel-Lindau Tumor Suppressor Gene Mutations Modulate Lipocalin-2 Expression in Ferroptotic-Inflammatory Pathways.Oxidative medicine and cellular longevity · 2023Article
- Development of Cell Therapies for Renal Disease and Regenerative Medicine.International journal of molecular sciences · 2022Review
- Astroglial and oligodendroglial markers in the cuprizone animal model for de- and remyelination.Histochemistry and cell biology · 2022Article
- Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022Review
- Review
- The Macrophage Iron Signature in Health and Disease.International journal of molecular sciences · 2021Review
- Macrophage-Derived Iron-Bound Lipocalin-2 Correlates with Renal Recovery Markers Following Sepsis-Induced Kidney Damage.International journal of molecular sciences · 2020Article
- Macrophage Phenotype and Fibrosis in Diabetic Nephropathy.International journal of molecular sciences · 2020Review
- Macrophage-secreted Lipocalin-2 Promotes Regeneration of Injured Primary Murine Renal Tubular Epithelial Cells.International journal of molecular sciences · 2020Article
- The iron load of lipocalin-2 (LCN-2) defines its pro-tumour function in clear-cell renal cell carcinoma.British journal of cancer · 2020Article
- CD4Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Exploring macrophage cell therapy on Diabetic Kidney Disease.Journal of cellular and molecular medicine · 2019Article
- The Impact of Versatile Macrophage Functions on Acute Kidney Injury and Its Outcomes.Frontiers in physiology · 2019Article
- Lipocalin-2 abrogates epithelial cell cycle arrest by PPARγ inhibition.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- A translational model of chronic kidney disease in swine.American journal of physiology. Renal physiology · 2018Article
- Administration of FTY720 during Tourniquet-Induced Limb Ischemia Reperfusion Injury Attenuates Systemic Inflammation.Mediators of inflammation · 2017Article
- Intracellular Iron Chelation Modulates the Macrophage Iron Phenotype with Consequences on Tumor Progression.PloS one · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal ischemia-reperfusion injury triggers an inflammatory response associated to infiltrating macrophages which determines the further outcome of disease. Brown Norway rats are known to show endogenous resistance to ischemia-induced renal damage. By contrast, Sprague Dawley rats exhibit a higher susceptibility to ischemic injury. In order to ascertain cytoprotective mechanisms, we focused on the implication of lipocalin-2 protein in main resistance mechanisms in renal ischemia/reperfusion injury by using adoptive macrophage administration, genetically modified ex vivo either to overexpress or to knockdown lipocalin-2. In vitro experiments with bone marrow-derived macrophages both from Brown Norway rats and from Sprague Dawley rats under hypoxic conditions showed endogenous differences regarding cytokine and lipocalin-2 expression profile in the two strains. Most interestingly, we observed that macrophages of the resistant strain express significantly more lipocalin-2. In vivo studies showed that tubular epithelial cell apoptosis and renal injury significantly increased and reparative markers decreased in Brown Norway rats after injection of lipocalin-2-knockdown macrophages, while the administration of lipocalin-2-overexpressing cells significantly decreased Sprague Dawley susceptibility. These data point to a crucial role of macrophage-derived lipocalin-2 in endogenous cytoprotective mechanisms. We conclude that expression of lipocalin-2 in tissue-infiltrating macrophages is pivotal for kidney-intrinsic cytoprotective pathways during ischemia reperfusion injury.
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