ArticlePloS one2015
Endothelial nitric oxide synthase deficient mice are protected from lipopolysaccharide induced acute lung injury.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- Ventilator-Induced Lung Injury: Mechanotransduction and Potential Therapeutic Targets.MedComm · 2026Review
- Nitration-driven structural changes in Hsp90 linked to gain of pathological functions.The Biochemical journal · 2025Article
- Endothelial cell dynamics in sepsis-induced acute lung injury and acute respiratory distress syndrome: pathogenesis and therapeutic implications.Cell communication and signaling : CCS · 2024Review
- The effects of iron deficient and high iron diets on SARS-CoV-2 lung infection and disease.Frontiers in microbiology · 2024Article
- Citrulline and ADI-PEG20 reduce inflammation in a juvenile porcine model of acute endotoxemia.Frontiers in immunology · 2024Article
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Glycosaminoglycans and fucoidan have a protective effect on experimental glomerulonephritis.Frontiers in molecular biosciences · 2023Article
- Time-Dependent Oxidative Alterations in Plasma and Lung Tissue after Meconium Aspiration in a Rabbit Model.Antioxidants (Basel, Switzerland) · 2022Article
- Different Transcutaneous Auricular Vagus Nerve Stimulation Parameters Modulate the Anti-Inflammatory Effects on Lipopolysaccharide-Induced Acute Inflammation in Mice.Biomedicines · 2022Article
- The role of oxidative stress in the pathogenesis of infections with coronaviruses.Frontiers in microbiology · 2022Review
- The protective effect of natural medicines against excessive inflammation and oxidative stress in acute lung injury by regulating the Nrf2 signaling pathway.Frontiers in pharmacology · 2022Review
- Bergamottin alleviates LPS-induced acute lung injury by inducing SIRT1 and suppressing NF-κB.Innate immunity · 2021Article
- Impairment of hypoxic pulmonary vasoconstriction in acute respiratory distress syndrome.European respiratory review : an official journal of the European Respiratory Society · 2021Review
- Article
- Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injury.Redox biology · 2021Article
- The Role of Ferroptosis in Acute Respiratory Distress Syndrome.Frontiers in medicine · 2021Review
- Endothelial Damage in Acute Respiratory Distress Syndrome.International journal of molecular sciences · 2020Review
- Biomechanical Forces and Oxidative Stress: Implications for Pulmonary Vascular Disease.Antioxidants & redox signaling · 2019Review
- Arginase impairs hypoxic pulmonary vasoconstriction in murine endotoxemia.Respiratory research · 2019Article
- Whole body periodic acceleration improves survival and microvascular leak in a murine endotoxin model.PloS one · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Lipopolysaccharide (LPS) derived from the outer membrane of gram-negative bacteria induces acute lung injury (ALI) in mice. This injury is associated with lung edema, inflammation, diffuse alveolar damage, and severe respiratory insufficiency. We have previously reported that LPS-mediated nitric oxide synthase (NOS) uncoupling, through increases in asymmetric dimethylarginine (ADMA), plays an important role in the development of ALI through the generation of reactive oxygen and nitrogen species. Therefore, the focus of this study was to determine whether mice deficient in endothelial NOS (eNOS-/-) are protected against ALI. In both wild-type and eNOS-/- mice, ALI was induced by the intratracheal instillation of LPS (2 mg/kg). After 24 hours, we found that eNOS-/-mice were protected against the LPS mediated increase in inflammatory cell infiltration, inflammatory cytokine production, and lung injury. In addition, LPS exposed eNOS-/- mice had increased oxygen saturation and improved lung mechanics. The protection in eNOS-/- mice was associated with an attenuated production of NO, NOS derived superoxide, and peroxynitrite. Furthermore, we found that eNOS-/- mice had less RhoA activation that correlated with a reduction in RhoA nitration at Tyr34. Finally, we found that the reduction in NOS uncoupling in eNOS-/- mice was due to a preservation of dimethylarginine dimethylaminohydrolase (DDAH) activity that prevented the LPS-mediated increase in ADMA. Together our data suggest that eNOS derived reactive species play an important role in the development of LPS-mediated lung injury.
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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.