ArticleStem cells (Dayton, Ohio)2016
The Oxygen Environment at Birth Specifies the Population of Alveolar Epithelial Stem Cells in the Adult Lung.
Article in Stem cells (Dayton, Ohio), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Inhibition of Cyclophilin D Rescues Cardiac Function and Bioenergetic Defects Caused by Neonatal Hypoxia.JACC. Basic to translational science · 2026Article
- Lineage Tracing of Distal Lung Epithelial Progenitors in Injury-Induced Regeneration.The clinical respiratory journal · 2025Review
- The cGAS-STING Pathway in Pulmonary Diseases: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2025Review
- The aging lung: microenvironment, mechanisms, and diseases.Frontiers in immunology · 2024Review
- Submersion and hypoxia inhibit alveolar epithelial NaRespiratory research · 2023Article
- Diacetyl inhalation impairs airway epithelial repair in mice infected with influenza A virus.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Lung Regeneration: Cells, Models, and Mechanisms.Cold Spring Harbor perspectives in biology · 2022Review
- Review
- 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
- Role of released mitochondrial DNA in acute lung injury.Frontiers in immunology · 2022Review
- Low-dose hyperoxia primes airways for fibrosis in mice after influenza A infection.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Neonatal hyperoxia impairs adipogenesis of bone marrow-derived mesenchymal stem cells and fat accumulation in adult mice.Free radical biology & medicine · 2021Article
- Loss of circadian protection against influenza infection in adult mice exposed to hyperoxia as neonates.eLife · 2021Article
- Airway Basal Cells Mediate Hypoxia-Induced EMT by Increasing Ribosome Biogenesis.Frontiers in pharmacology · 2021Article
- Effects of Hyperoxia on Mitochondrial Homeostasis: Are Mitochondria the Hub for Bronchopulmonary Dysplasia?Frontiers in cell and developmental biology · 2021Review
- Small GTPase RAB6 deficiency promotes alveolar progenitor cell renewal and attenuates PM2.5-induced lung injury and fibrosis.Cell death & disease · 2020Article
- Alveolar regeneration through a Krt8+ transitional stem cell state that persists in human lung fibrosis.Nature communications · 2020Article
- Negative impact of hyperglycaemia on mouse alveolar development.Cell cycle (Georgetown, Tex.) · 2018Article
- Alternative Progenitor Lineages Regenerate the Adult Lung Depleted of Alveolar Epithelial Type 2 Cells.American journal of respiratory cell and molecular biology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Alveolar epithelial type II cells (AEC2) maintain pulmonary homeostasis by producing surfactant, expressing innate immune molecules, and functioning as adult progenitor cells for themselves and alveolar epithelial type I cells (AEC1). How the proper number of alveolar epithelial cells is determined in the adult lung is not well understood. Here, BrdU labeling, genetic lineage tracing, and targeted expression of the anti-oxidant extracellular superoxide dismutase in AEC2s are used to show how the oxygen environment at birth influences postnatal expansion of AEC2s and AEC1s in mice. Birth into low (12%) or high (≥60%) oxygen stimulated expansion of AEC2s through self-renewal and differentiation of the airway Scgb1a1 + lineage. This non-linear or hormesis response to oxygen was specific for the alveolar epithelium because low oxygen stimulated and high oxygen inhibited angiogenesis as defined by changes in V-cadherin and PECAM (CD31). Although genetic lineage tracing studies confirmed adult AEC2s are stem cells for AEC1s, we found no evidence that postnatal growth of AEC1s were derived from self-renewing Sftpc + or the Scbg1a1 + lineage of AEC2s. Taken together, our results show how a non-linear response to oxygen at birth promotes expansion of AEC2s through two distinct lineages. Since neither lineage contributes to the postnatal expansion of AEC1s, the ability of AEC2s to function as stem cells for AEC1s appears to be restricted to the adult lung. Stem Cells 2016;34:1396-1406.
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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 OpenQuestion graph.