ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Neonatal oxygen adversely affects lung function in adult mice without altering surfactant composition or activity.
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 94 papers.
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Who cites it
94 citing papers in PubMed, 123 citations in OpenAlex.
- Intranasal delivery of human umbilical cord Wharton's jelly mesenchymal stromal cells restores lung alveolarization and vascularization in experimental bronchopulmonary dysplasia.Stem cells translational medicine · 2020Trial
- Attenuation of Experimental Bronchopulmonary Dysplasia by Dimethyl Fumarate.Pediatric research · 2026Article
- Non-invasive respiratory support attenuates lung damage in a murine model of bronchopulmonary dysplasia.Frontiers in pediatrics · 2026Article
- Preterm Birth Conditions Alter Muscle Stem Cells and Their Niche, Causing Lasting Impairments in Muscle Regeneration and Function.Journal of cachexia, sarcopenia and muscle · 2025Article
- Systemic heparin administration impairs lung development in neonatal mice.Scientific reports · 2025Article
- Whole genome transcriptomics reveal distinct atrial versus ventricular responses to neonatal hyperoxia.American journal of physiology. Heart and circulatory physiology · 2025Article
- Impaired myofibroblast proliferation is a central feature of pathologic post-natal alveolar simplification.eLife · 2024Article
- Decreased Liver Kinase B1 Expression and Impaired Angiogenesis in a Murine Model of Bronchopulmonary Dysplasia.American journal of respiratory cell and molecular biology · 2024Article
- Impaired Myofibroblast Proliferation is a Central Feature of Pathologic Post-Natal Alveolar Simplification.bioRxiv : the preprint server for biology · 2024Article
- PD-1 signaling in neonates restrains CD8Mucosal immunology · 2024Article
- Article
- Timing and cell specificity of senescence drives postnatal lung development and injury.Nature communications · 2023Article
- Oxygen and mechanical stretch in the developing lung: risk factors for neonatal and pediatric lung disease.Frontiers in medicine · 2023Review
- Diacetyl inhalation impairs airway epithelial repair in mice infected with influenza A virus.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Upregulating carnitine palmitoyltransferase 1 attenuates hyperoxia-induced endothelial cell dysfunction and persistent lung injury.Respiratory research · 2022Article
- SM22α cell-specific HIF stabilization mitigates hyperoxia-induced neonatal lung injury.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Macrophage-derived IL-6 trans-signalling as a novel target in the pathogenesis of bronchopulmonary dysplasia.The European respiratory journal · 2022Article
- Single-cell transcriptomics reveals lasting changes in the lung cellular landscape into adulthood after neonatal hyperoxic exposure.Redox biology · 2021Article
- Age-dependent alveolar epithelial plasticity orchestrates lung homeostasis and regeneration.Cell stem cell · 2021Article
- Neonatal hyperoxia impairs adipogenesis of bone marrow-derived mesenchymal stem cells and fat accumulation in adult mice.Free radical biology & medicine · 2021Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
Despite its potentially adverse effects on lung development and function, supplemental oxygen is often used to treat premature infants in respiratory distress. To understand how neonatal hyperoxia can permanently disrupt lung development, we previously reported increased lung compliance, greater alveolar simplification, and disrupted epithelial development in adult mice exposed to 100% inspired oxygen fraction between postnatal days 1 and 4. Here, we investigate whether oxygen-induced changes in lung function are attributable to defects in surfactant composition and activity, structural changes in alveolar development, or both. Newborn mice were exposed to room air or 40%, 60%, 80%, or 100% oxygen between postnatal days 1 and 4 and allowed to recover in room air until 8 wk of age. Lung compliance and alveolar size increased, and airway resistance, airway elastance, tissue elastance, and tissue damping decreased, in mice exposed to 60-80% oxygen; changes were even greater in mice exposed to 100% oxygen. These alterations in lung function were not associated with changes in total protein content or surfactant phospholipid composition in bronchoalveolar lavage. Moreover, surface activity and total and hydrophobic protein content were unchanged in large surfactant aggregates centrifuged from bronchoalveolar lavage compared with control. Instead, the number of type II cells progressively declined in 60-100% oxygen, whereas levels of T1alpha, a protein expressed by type I cells, were comparably increased in mice exposed to 40-100% oxygen. Thickened bundles of elastin fibers were also detected in alveolar walls of mice exposed to > or = 60% oxygen. These findings support the hypothesis that changes in lung development, rather than surfactant activity, are the primary causes of oxygen-altered lung function in children who were exposed to oxygen as neonates. Furthermore, the disruptive effects of oxygen on epithelial development and lung mechanics are not equivalently dose dependent.
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