ArticlePediatric research2015
Lack of EC-SOD worsens alveolar and vascular development in a neonatal mouse model of bleomycin-induced bronchopulmonary dysplasia and pulmonary hypertension.
Article in Pediatric research, 2015. 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, 38 citations in OpenAlex.
- R213G-Mediated Redistribution of EC-SOD Protects Against Sugen-Hypoxia Pulmonary Hypertension in Mice.Pulmonary circulation · 2026Article
- Vascular EC-SOD limits the accumulation, proinflammatory profibrotic reprogramming, and hyaluronan binding of interstitial macrophages in hypoxia.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Review
- A maternal hypoxia mouse model to study the effect of late gestational hypoxia on offspring lung outcomes.Frontiers in physiology · 2025Article
- Research progress of microvascular development in bronchopulmonary dysplasia.Pediatric investigation · 2024Review
- Redistribution of SOD3 expression due to R213G polymorphism affects pulmonary interstitial macrophage reprogramming in response to hypoxia.Physiological genomics · 2024Article
- Lung EC-SOD Overexpression Prevents Hypoxia-Induced Platelet Activation and Lung Platelet Accumulation.Antioxidants (Basel, Switzerland) · 2024Article
- Strategies for the prevention of bronchopulmonary dysplasia.Frontiers in pediatrics · 2024Review
- Role of Postnatal Corticosteroids in the Treatment or Prevention of Bronchopulmonary Dysplasia.Sisli Etfal Hastanesi tip bulteni · 2023Review
- Neonatal Selenium Deficiency Decreases Selenoproteins in the Lung and Impairs Pulmonary Alveolar Development.Antioxidants (Basel, Switzerland) · 2022Article
- Pharmacotherapy in Bronchopulmonary Dysplasia: What Is the Evidence?Frontiers in pediatrics · 2022Review
- Patho-mechanisms of the origins of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2021Review
- Neonatal Extracellular Superoxide Dismutase Knockout Mice Increase Total Superoxide Dismutase Activity and VEGF Expression after Chronic Hyperoxia.Antioxidants (Basel, Switzerland) · 2021Article
- Phenotypes of Bronchopulmonary Dysplasia.International journal of molecular sciences · 2020Review
- Platelet activation in experimental murine neonatal pulmonary hypertension.Physiological reports · 2020Article
- Anti-oxidative effects of superoxide dismutase 3 on inflammatory diseases.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Lung-Derived SOD3 Attenuates Neurovascular Injury After Transient Global Cerebral Ischemia.Journal of the American Heart Association · 2019Article
- Recent Advances in Studies of Molecular Hydrogen against Sepsis.International journal of biological sciences · 2019Review
- Role of SOD3 in silica-related lung fibrosis and pulmonary vascular remodeling.Respiratory research · 2018Article
- Serotonin 2A receptor inhibition protects against the development of pulmonary hypertension and pulmonary vascular remodeling in neonatal mice.American journal of physiology. Lung cellular and molecular physiology · 2018Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPulmonary hypertension (PH) worsens clinical outcomes in former preterm infants with bronchopulmonary dysplasia (BPD). Oxidant stress disrupts alveolar and vascular development in models of BPD. Bleomycin causes oxidative stress and induces BPD and PAH in neonatal rats. Disruption in the vascular endothelial growth factor (VEGF) and nitric oxide signaling pathways contributes to BPD. We hypothesized that loss of EC-SOD would worsen PAH associated with BPD in a neonatal mouse model of bleomycin-induced BPD by disrupting the VEGF/NO signaling pathway.
methodsNeonatal wild-type mice (WT), and mice lacking EC-SOD (EC-SOD KO) received intraperitoneal bleomycin (2 units/kg) or phosphate-buffered saline (PBS) three times weekly and were evaluated at weeks 3 or 4.
resultsLack of EC-SOD impaired alveolar development and resulted in PH (elevated right ventricular systolic pressures, right ventricular hypertrophy (RVH)), decreased vessel density, and increased small vessel muscularization. Exposure to bleomycin further impaired alveolar development, worsened RVH and vascular remodeling. Lack of EC-SOD and bleomycin treatment decreased lung total and phosphorylated VEGFR2 and eNOS protein expression.
conclusionEC-SOD is critical in preserving normal lung development and loss of EC-SOD results in disrupted alveolar development, PAH and vascular remodeling at baseline, which is further worsened with bleomycin and associated with decreased activation of VEGFR2.
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