2014
DOI: 10.1165/rcmb.2013-0207oc
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Neonatal Hyperoxia Stimulates the Expansion of Alveolar Epithelial Type II Cells

Abstract: Supplemental oxygen used to treat infants born prematurely disrupts angiogenesis and is a risk factor for persistent pulmonary disease later in life. Although it is unclear how neonatal oxygen affects development of the respiratory epithelium, alveolar simplification and depletion of type II cells has been observed in adult mice exposed to hyperoxia between postnatal Days 0 and 4. Because hyperoxia inhibits cell proliferation, we hypothesized that it depleted the adult lung of type II cells by inhibiting their… Show more

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Cited by 56 publications
(54 citation statements)
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“…In vitro, hyperoxia induces apoptotic and necrotic AEC death 141, 142 , and promotes type II AEC (AECII) differentiation to a type I AEC (AECI) phenotype 143 . In vivo, hyperoxia induces rapid expansion of AECII in the neonatal lung, which are quickly depleted during recovery, resulting in fewer AECII in the adult lung, and potentially contributing to the emphysema observed in adult mice exposed to perinatal hyperoxia 144, 145 . Of note, hyperoxia also re-induces telomerase activity in mature AECII, providing support for the notion that AECII may serve as population of resident progenitors after injury 146 .…”
Section: Disruption Of Essential Developmental Pathwaysmentioning
confidence: 99%
“…In vitro, hyperoxia induces apoptotic and necrotic AEC death 141, 142 , and promotes type II AEC (AECII) differentiation to a type I AEC (AECI) phenotype 143 . In vivo, hyperoxia induces rapid expansion of AECII in the neonatal lung, which are quickly depleted during recovery, resulting in fewer AECII in the adult lung, and potentially contributing to the emphysema observed in adult mice exposed to perinatal hyperoxia 144, 145 . Of note, hyperoxia also re-induces telomerase activity in mature AECII, providing support for the notion that AECII may serve as population of resident progenitors after injury 146 .…”
Section: Disruption Of Essential Developmental Pathwaysmentioning
confidence: 99%
“…A possible explanation for these primary and subsequent phenotypes is that neonatal hyperoxia reduces numbers of alveolar epithelial AT2 cells [46], which are known to serve as progenitor cells during alveologenesis and alveolar repair [73]. Although it is possible that Trx2 mediates AT2 cell death in vivo , it is unlikely that hyperoxic depletion of AT2 cells in the perinatal lung can be explained exclusively by cell death.…”
Section: Discussionmentioning
confidence: 99%
“…Although it is possible that Trx2 mediates AT2 cell death in vivo , it is unlikely that hyperoxic depletion of AT2 cells in the perinatal lung can be explained exclusively by cell death. Yee et al report that hyperoxia stimulates expression of genetic markers indicative of alveologenesis and that AT2 cell numbers slowly diminish during the recovery phase [6]. This exacerbated expansion of AT2 cells may be due to prolonged or enhanced activation of oxygen-dependent signaling pathways regulating perinatal alveologenesis while transitioning to a more oxidative atmospheric environment outside the womb.…”
Section: Discussionmentioning
confidence: 99%
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“…In recent work by the same group, the authors observed a significant AEC2 expansion immediately after neonatal hypoxia/hyperoxia that not only does not persist, but actually declines, leading to an overall reduction in AEC2 numbers in the adult (17,18). Furthermore, AEC2-like cells arise in the airways of mice exposed to hypoxia/hyperoxia at birth after viral infection as adults but do not appear to contribute to alveolar maintenance.…”
mentioning
confidence: 97%