ArticleThe American journal of pathology2014
Lung development alterations in newborn mice after recovery from exposure to sublethal hyperoxia.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Deficiency of Secreted Phosphoprotein 1 Alleviates Hyperoxia-induced Bronchopulmonary Dysplasia in Neonatal Mice.Inflammation · 2025Article
- Oxygen Toxicity to the Immature Lung-Part II: The Unmet Clinical Need for Causal Therapy.International journal of molecular sciences · 2021Review
- Fully automated estimation of the mean linear intercept in histopathology images of mouse lung tissue.Journal of medical imaging (Bellingham, Wash.) · 2021Article
- Intratracheal Keratinocyte Growth Factor Enhances Surfactant Protein B Expression in Mechanically Ventilated Preterm Pigs.Frontiers in pediatrics · 2021Article
- Mechanisms of Impaired Lung Development and Ciliation in Mannosidase-1-Alpha-2 (Frontiers in physiology · 2021Article
- Neonatal hyperoxia promotes asthma-like features through IL-33-dependent ILC2 responses.The Journal of allergy and clinical immunology · 2018Article
- Neonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization in adulthood.Scientific reports · 2017Article
- Looking ahead: where to next for animal models of bronchopulmonary dysplasia?Cell and tissue research · 2017Review
- Aberrant cGMP signaling persists during recovery in mice with oxygen-induced pulmonary hypertension.PloS one · 2017Article
- Pathogenesis of bronchopulmonary dysplasia: when inflammation meets organ development.Molecular and cellular pediatrics · 2016Review
- Impact of bronchopulmonary dysplasia on brain and retina.Biology open · 2016Article
- Article
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9 authors.
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Abstract
Exposure of newborn mice to hyperoxia arrests lung development, with resultant pathological characteristics similar to bronchopulmonary dysplasia in infants born prematurely. We tested the hypothesis that aberrations in lung development caused by 14 days of sublethal hyperoxia would be reversed during 14 days of recovery to room air (RA) when the concentration of oxygen exposure was weaned gradually. Newborn FVB mice were exposed to 85% oxygen or RA for 14 days. Weaning from hyperoxia was by either transfer directly into RA or a decrease in the concentration of oxygen by 10% per days. At 28 days, pups were euthanized, and the lungs were inflation fixed and assessed. At postnatal day 28, lungs of mice weaned abruptly from hyperoxia had fewer (6 ± 0.6 versus 10 ± 0.7; P < 0.001) alveoli per high-powered field and larger alveoli (4050 ± 207 versus 2305 ± 182 μm(2)) than animals weaned gradually; both hyperoxia-exposed groups were different from lungs obtained from air-breathing controls (20 ± 0.5 alveoli per high-powered field; P < 0.001). The results are consistent with the absence of catch-up alveolarization in this model and indicate that the long-term consequences of early exposures to hyperoxia merit closer examination. The effects of abrupt weaning to RA observed further suggest that weaning should be considered in experimental models of newborn exposure to hyperoxia.
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