ArticlePloS one2011
Pulmonary oxidative stress is increased in cyclooxygenase-2 knockdown mice with mild pulmonary hypertension induced by monocrotaline.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 49 citations in OpenAlex.
- The chemical composition of secondary organic aerosols regulates transcriptomic and metabolomic signaling in an epithelial-endothelial in vitro coculture.Particle and fibre toxicology · 2024Article
- Prostaglandin and prostaglandin receptors: present and future promising therapeutic targets for pulmonary arterial hypertension.Respiratory research · 2023Review
- Cannabidiol Improves Antioxidant Capacity and Reduces Inflammation in the Lungs of Rats with Monocrotaline-Induced Pulmonary Hypertension.Molecules (Basel, Switzerland) · 2022Article
- Oxidized LDL-dependent pathway as new pathogenic trigger in arrhythmogenic cardiomyopathy.EMBO molecular medicine · 2021Article
- Pediatric Pulmonary Hypertension: Definitions, Mechanisms, Diagnosis, and Treatment.Comprehensive Physiology · 2021Article
- Exposure Effects Beyond the Epithelial Barrier: Transepithelial Induction of Oxidative Stress by Diesel Exhaust Particulates in Lung Fibroblasts in an Organotypic Human Airway Model.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Vascular Metabolic Mechanisms of Pulmonary Hypertension.Current medical science · 2020Review
- β3 adrenergic receptor antagonist SR59230A exerts beneficial effects on right ventricular performance in monocrotaline-induced pulmonary arterial hypertension.Experimental and therapeutic medicine · 2020Article
- Redox Regulation of Ion Channels and Receptors in Pulmonary Hypertension.Antioxidants & redox signaling · 2019Review
- Effect of a phosphodiesterase-5A (PDE5A) gene polymorphism on response to sildenafil therapy in canine pulmonary hypertension.Scientific reports · 2019Article
- Regulation of Smooth Muscle Cell Proliferation by NADPH Oxidases in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2019Review
- Anti-oxidants correct disturbance of redox enzymes in the hearts of rat fetuses with congenital diaphragmatic hernia.Pediatric surgery international · 2018Article
- Reactive Oxygen and Nitrogen Species in the Development of Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2017Review
- Effects of aerobic exercise training on metabolism of nitric oxide and endothelin-1 in lung parenchyma of rats with pulmonary arterial hypertension.Molecular and cellular biochemistry · 2017Article
- Possible role of increased oxidative stress in pulmonary hypertension in experimental diaphragmatic hernia.Pediatric surgery international · 2016Article
- EP3 receptor deficiency attenuates pulmonary hypertension through suppression of Rho/TGF-β1 signaling.The Journal of clinical investigation · 2015Article
- Increased eicosanoid levels in the Sugen/chronic hypoxia model of severe pulmonary hypertension.PloS one · 2015Article
- Intratracheal administration of cyclooxygenase-1-transduced adipose tissue-derived stem cells ameliorates monocrotaline-induced pulmonary hypertension in rats.American journal of physiology. Heart and circulatory physiology · 2014Article
- Organ specific optical imaging of mitochondrial redox state in a rodent model of hereditary hemorrhagic telangiectasia-1.Journal of biophotonics · 2014Article
- A novel p38 mitogen-activated protein kinase/Elk-1 transcription factor-dependent molecular mechanism underlying abnormal endothelial cell proliferation in plexogenic pulmonary arterial hypertension.The Journal of biological chemistry · 2013Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The aim of this study was to examine the role of cyclooxygenase-2 (COX-2) and downstream signaling of prostanoids in the pathogenesis of pulmonary hypertension (PH) using mice with genetically manipulated COX-2 expression. COX-2 knockdown (KD) mice, characterized by 80-90% suppression of COX-2, and wild-type (WT) control mice were treated weekly with monocrotaline (MCT) over 10 weeks. Mice were examined for cardiac hypertrophy/function and right ventricular pressure. Lung histopathological analysis was performed and various assays were carried out to examine oxidative stress, as well as gene, protein, cytokine and prostanoid expression. We found that MCT increased right ventricular systolic and pulmonary arterial pressures in comparison to saline-treated mice, with no evidence of cardiac remodeling. Gene expression of endothelin receptor A and thromboxane synthesis, regulators of vasoconstriction, were increased in MCT-treated lungs. Bronchoalveolar lavage fluid and lung sections demonstrated mild inflammation and perivascular edema but activation of inflammatory cells was not predominant under the experimental conditions. Heme oxygenase-1 (HO-1) expression and indicators of oxidative stress in lungs were significantly increased, especially in COX-2 KD MCT-treated mice. Gene expression of NOX-4, but not NOX-2, two NADPH oxidase subunits crucial for superoxide generation, was induced by ∼4-fold in both groups of mice by MCT. Vasodilatory and anti-aggregatory prostacyclin was reduced by ∼85% only in MCT-treated COX-2 KD mice. This study suggests that increased oxidative stress-derived endothelial dysfunction, vasoconstriction and mild inflammation, exacerbated by the lack of COX-2, contribute to the pathogenesis of early stages of PH when mild hemodynamic changes are evident and not yet accompanied by vascular and cardiac remodeling.
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