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1 Pediatrics, The University of Rochester, Rochester, New York, United States
2 Environmental Medicine, The University of Rochester, Rochester, New York, United States
3 Pediatrics, Johns Hopkins University, Baltimore, Maryland, United States
4 Pediatrics, The University of Rochester, Rochester, New York, United States; Pediatrics, University Rochester School Medicine Dentistry, Rochester, New York, United States
5 Pediatrics, University of Rochester, Rochester, New York, United States
* To whom correspondence should be addressed. E-mail: michael_oreilly{at}urmc.rochester.edu.
Type II epithelial cells are essential for lung development and remodeling, as they are precursors for type I cells and can produce vascular mitogens. While type II cell proliferation takes place following hyperoxia, it is unclear why alveolar remodeling occurs normally in adults while it is permanently disrupted in newborns. Using a line of transgenic mice whose type II cells could be identified by their expression of EGFP and endogenous expression of surfactant proteins, the age-dependent effects of hyperoxia on type II cell proliferation and alveolar repair were investigated. In adult mice, type II cell proliferation was low during room and hyperoxia, while increasing during recovery in room air and then declining to control levels by day 7. Eight weeks later, type II cell number and alveolar compliance were indistinguishable from room air controls. In newborn mice, type II cell proliferation markedly increased between birth and postnatal day 7 before declining by day 14. Exposure to hyperoxia between postnatal days 1 and 4 inhibited type II cell proliferation, which resumed during recovery and was aberrantly elevated on day 14. Eight weeks later, recovered mice had 70% fewer type II cells and 30% increased lung compliance compared to controls. Recovered mice also had higher levels of T1
, a protein expressed by type I cells, with minimal changes detected in genes expressed by vascular cells. These data suggest perinatal hyperoxia adversely affects alveolar development by disrupting the proper timing of type II cell proliferation and differentiation into type I cells.
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