ArticleAmerican journal of physiology. Heart and circulatory physiology2015
Right ventricular cyclic nucleotide signaling is decreased in hyperoxia-induced pulmonary hypertension in neonatal mice.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Hyperoxia and pulmonary vascular injury in bronchopulmonary dysplasia: pathogenic mechanisms and emerging therapies-a systematic review.Pediatric research · 2026Pooled it
- Endothelial Cpt1a Inhibits Neonatal Hyperoxia-Induced Pulmonary Vascular Remodeling by Repressing Endothelial-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Evidence-Based Guidelines for Acute Stabilization and Management of Neonates with Persistent Pulmonary Hypertension of the Newborn.American journal of perinatology · 2023Article
- Development of a novel humanized mouse model to study bronchopulmonary dysplasia.Frontiers in pediatrics · 2023Article
- Pediatric Pulmonary Hypertension: Definitions, Mechanisms, Diagnosis, and Treatment.Comprehensive Physiology · 2021Article
- Interactive and independent effects of early lipopolysaccharide and hyperoxia exposure on developing murine lungs.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Therapies that enhance pulmonary vascular NO-signaling in the neonate.Nitric oxide : biology and chemistry · 2020Review
- Lung omics signatures in a bronchopulmonary dysplasia and pulmonary hypertension-like murine model.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Aberrant cGMP signaling persists during recovery in mice with oxygen-induced pulmonary hypertension.PloS one · 2017Article
- Altered Right Ventricular Mechanical Properties Are Afterload Dependent in a Rodent Model of Bronchopulmonary Dysplasia.Frontiers in physiology · 2017Article
- Dose-dependent effects of glucocorticoids on pulmonary vascular development in a murine model of hyperoxic lung injury.Pediatric research · 2016Article
- Phenotypic assessment of pulmonary hypertension using high-resolution echocardiography is feasible in neonatal mice with experimental bronchopulmonary dysplasia and pulmonary hypertension: a step toward preventing chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2016Article
- Mouse lung development and NOX1 induction during hyperoxia are developmentally regulated and mitochondrial ROS dependent.American journal of physiology. Lung cellular and molecular physiology · 2015Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Pulmonary hypertension (PH) and right ventricular hypertrophy (RVH) affect 25-35% of premature infants with significant bronchopulmonary dysplasia (BPD), increasing morbidity and mortality. We sought to determine the role of phosphodiesterase 5 (PDE5) in the right ventricle (RV) and left ventricle (LV) in a hyperoxia-induced neonatal mouse model of PH and RVH. After birth, C57BL/6 mice were placed in room air (RA) or 75% O2 (CH) for 14 days to induce PH and RVH. Mice were euthanized at 14 days or recovered in RA for 14 days or 42 days prior to euthanasia at 28 or 56 days of age. Some pups received sildenafil or vehicle (3 mg·kg(-1)·dose(-1) sc) every other day from P0. RVH was assessed by Fulton's index [RV wt/(LV + septum) wt]. PDE5 protein expression was analyzed via Western blot, PDE5 activity was measured by commercially available assay, and cGMP was measured by enzyme-linked immunoassay. Hyperoxia induced RVH in mice after 14 days, and RVH did not resolve until 56 days of age. Hyperoxia increased PDE5 expression and activity in RV, but not LV + S, after 14 days. PDE5 expression normalized by 28 days of age, but PDE5 activity did not normalize until 56 days of age. Sildenafil given during hyperoxia prevented RVH, decreased RV PDE5 activity, and increased RV cGMP levels. Mice with cardiac-specific overexpression of PDE5 had increased RVH in RA. These findings suggest normal RV PDE5 function is disrupted by hyperoxia, and elevated PDE5 contributes to RVH and remodeling. Therefore, in addition to impacting the pulmonary vasculature, sildenafil also targets PDE5 in the neonatal mouse RV and decreases RVH.
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