ArticlePloS one2014
Arginase-1 deficiency regulates arginine concentrations and NOS2-mediated NO production during endotoxemia.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- L-Arginine and Its Metabolites in Age-Related Cerebral Small Vessel Disease with Cognitive Impairment.Biomolecules · 2026Article
- Macrophage-intrinsic and IL-9-dependent arginine metabolism promotes lung tumor growth.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Arginine metabolism in myeloid cells in health and disease.Seminars in immunopathology · 2025Review
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- Fructose: a modulator of intestinal barrier function and hepatic health?European journal of nutrition · 2023Review
- Multi-Omics Endotypes in ICU Sepsis-Induced Immunosuppression.Microorganisms · 2023Review
- Endothelial cell metabolism in sepsis.World journal of emergency medicine · 2023Review
- Arginine Availability in Reamed Intramedullary Aspirate as Predictor of Outcome in Nonunion Healing.Biomedicines · 2022Article
- Alterations of nitric oxide homeostasis as trigger of intestinal barrier dysfunction in non-alcoholic fatty liver disease.Journal of cellular and molecular medicine · 2022Article
- H1N1 Influenza Virus-Infected Nasal Mucosal Epithelial Progenitor Cells Promote Dendritic Cell Recruitment and Maturation.Frontiers in immunology · 2022Article
- Microcirculatory Function during Endotoxemia-A Functional Citrulline-Arginine-NO Pathway and NOS3 Complex Is Essential to Maintain the Microcirculation.International journal of molecular sciences · 2021Article
- Regulation of T Cells in Cancer by Nitric Oxide.Cells · 2021Review
- Activated M1 macrophages suppress c-kit expression via TNF-α-mediated upregulation of miR-222 in Neonatal Necrotizing Enterocolitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- The acidified drinking water-induced changes in the behavior and gut microbiota of wild-type mice depend on the acidification mode.Scientific reports · 2021Article
- Pathological Features of Enterovirus 71-Associated Brain and Lung Damage in Mice Based on Quantitative Proteomic Analysis.Frontiers in microbiology · 2021Article
- TLR signaling adapter BCAP regulates inflammatory to reparatory macrophage transition by promoting histone lactylation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Arginine and Endothelial Function.Biomedicines · 2020Review
- Derangement of Arginine and Related Amino Acids in Children Undergoing Surgery for Congenital Heart Disease With Cardiopulmonary Bypass.Critical care explorations · 2020Article
- Bench to bedside review: therapeutic modulation of nitric oxide in sepsis-an update.Intensive care medicine experimental · 2019Review
- Immunometabolism and Sepsis: A Role for HIF?Frontiers in molecular biosciences · 2019Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RATIONALE AND
objectiveArginase-1 is an important component of the intricate mechanism regulating arginine availability during immune responses and nitric oxide synthase (NOS) activity. In this study Arg1(fl/fl)/Tie2-Cre(tg/-) mice were developed to investigate the effect of arginase-1 related arginine depletion on NOS2- and NOS3-dependent NO production and jejunal microcirculation under resting and endotoxemic conditions, in mice lacking arginase-1 in endothelial and hematopoietic cells. METHODS AND
resultsArginase-1-deficient mice as compared with control mice exhibited higher plasma arginine concentration concomitant with enhanced NO production in endothelial cells and jejunal tissue during endotoxemia. In parallel, impaired jejunal microcirculation was observed in endotoxemic conditions. Cultured bone-marrow-derived macrophages of arginase-1 deficient animals also presented a higher inflammatory response to endotoxin than control littermates. Since NOS2 competes with arginase for their common substrate arginine during endotoxemia, Nos2 deficient mice were also studied under endotoxemic conditions. As Nos2(-/-) macrophages showed an impaired inflammatory response to endotoxin compared to wild-type macrophages, NOS2 is potentially involved. A strongly reduced NO production in Arg1(fl/fl)/Tie2-Cre(tg/-) mice following infusion of the NOS2 inhibitor 1400W further implicated NOS2 in the enhanced capacity to produce NO production Arg1(fl/fl)/Tie2-Cre(tg/-) mice.
conclusionsReduced arginase-1 activity in Arg1(fl/fl)/Tie2-Cre(tg/-) mice resulted in increased inflammatory response and NO production by NOS2, accompanied by a depressed microcirculatory flow during endotoxemia. Thus, arginase-1 deficiency facilitates a NOS2-mediated pro-inflammatory activity at the expense of NOS3-mediated endothelial relaxation.
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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.