ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Hyperoxia impairs postnatal alveolar epithelial development via NADPH oxidase in newborn mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Molecular mechanisms underlying methotrexate-induced intestinal injury and protective strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Recombinant CXCL17 Treatment Alleviates Hyperoxia-Induced Lung Apoptosis and Inflammation In Vivo and Vitro by Activating the AKT Pathway: A Possible Therapeutic Approach for Bronchopulmonary Dysplasia.Molecular biotechnology · 2024Article
- Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.Cell biology and toxicology · 2023Review
- Early Origins of Chronic Obstructive Pulmonary Disease: Prenatal and Early Life Risk Factors.International journal of environmental research and public health · 2023Review
- Galantamine ameliorates hyperoxia-induced brain injury in neonatal mice.Frontiers in neuroscience · 2023Article
- Neonatal Hyperoxia Activates Activating Transcription Factor 4 to Stimulate Folate Metabolism and Alveolar Epithelial Type 2 Cell Proliferation.American journal of respiratory cell and molecular biology · 2022Article
- Preventable ATII Proliferation after Hyperoxia: The "Tempo" of Folate Metabolism in the Neonatal Lung.American journal of respiratory cell and molecular biology · 2022Article
- The Role of Sphingolipid Signaling in Oxidative Lung Injury and Pathogenesis of Bronchopulmonary Dysplasia.International journal of molecular sciences · 2022Review
- Alveolar type 2 epithelial cell senescence and radiation-induced pulmonary fibrosis.Frontiers in cell and developmental biology · 2022Review
- Molecular Mechanism of Caffeine in Preventing Bronchopulmonary Dysplasia in Premature Infants.Frontiers in pediatrics · 2022Review
- Effects of Hyperoxia on Mitochondrial Homeostasis: Are Mitochondria the Hub for Bronchopulmonary Dysplasia?Frontiers in cell and developmental biology · 2021Review
- Neonatal hyperoxia enhances age-dependent expression of SARS-CoV-2 receptors in mice.Scientific reports · 2020Article
- Prevention of Oxygen-Induced Inflammatory Lung Injury by Caffeine in Neonatal Rats.Oxidative medicine and cellular longevity · 2020Article
- Bronchopulmonary dysplasia: clinical aspects and preventive and therapeutic strategies.Journal of translational medicine · 2018Review
- Hyperoxia-induced p47phox activation and ROS generation is mediated through S1P transporter Spns2, and S1P/S1P1&2 signaling axis in lung endothelium.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- [17β‑estradiol suppresses hyperoxia‑induced apoptosis of oligodendrocyte precursor cells through paired‑immunoglobulin‑like receptor B].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
- Article
- 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
- A breath of fresh air on the mesenchyme: impact of impaired mesenchymal development on the pathogenesis of bronchopulmonary dysplasia.Frontiers in medicine · 2015Review
- Oxidative stress and inflammation modulate Rev-erbα signaling in the neonatal lung and affect circadian rhythmicity.Antioxidants & redox signaling · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hyperoxia disrupts postnatal lung development in part through inducing inflammation. To determine the contribution of leukocyte-derived reactive oxygen species, we exposed newborn wild-type and NADPH oxidase p47(phox) subunit null (p47(phox-/-)) mice to air or acute hyperoxia (95% O(2)) for up to 11 days. Hyperoxia-induced pulmonary neutrophil influx was similar in wild-type and p47(-/-) mice at postnatal days (P) 7 and 11. Macrophages were decreased in wild-type hyperoxia-exposed mice compared with p47(phox-/-) mice at P11. Hyperoxia impaired type II alveolar epithelial cell and bronchiolar epithelial cell proliferation, but depression of type II cell proliferation was significantly less in p47(-/-) mice at P3 and P7, when inflammation was minimal. We found reciprocal results for the expression of the cell cycle inhibitor p21(cip/waf) in type II cells, which was induced in 95% O(2)-exposed wild-type mice, but significantly less in p47(phox-/-) littermates at P7. Despite partial preservation of type II cell proliferation, deletion of p47(phox) did not prevent the major adverse effects of hyperoxia on alveolar development estimated by morphometry at P11, but hyperoxia impairment of elastin deposition at alveolar septal crests was significantly worse in wild-type vs. p47(phox-/-) mice at P11. Since we found that p47(phox) is expressed in a subset of alveolar epithelial cells, its deletion may protect postnatal type II alveolar epithelial proliferation from hyperoxia through effects on epithelial as well as phagocyte-generated superoxide.
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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 Socratic graph.