title: Altered expressions of fibroblast growth factor receptors and alveolarization in neonatal mice exposed to 85% oxygen.
abstract: In the present study, we tested the hypothesis that exposure of newborn mice to sublethal hyperoxia would alter lung development and expressions of fibroblast growth factor receptors (FGFRs)-3 and FGFR-4. Newborn FVB mice were exposed to 85% O2 or maintained in room air for up to 14 d. No animal mortality was observed, and body weight gains were not affected by hyperoxia. At postnatal d 7 and 14 (P7, P14), lungs of mice exposed to 85% O2 showed fewer alveolar secondary crests and larger alveoli or terminal air spaces than did mice in room air. In pups kept in room air, lung levels of FGFR-3 and FGFR-4 mRNA were greater at P3 than at P1, but similar increases were not observed in hyperoxic mice. Immunoreactivity of FGFR-3 and FGFR-4 was lower in lungs of hyperoxic mice than in controls at P14. In pups kept in room air, lung fibroblast growth factor (FGF)-7 mRNA levels were greater at P14 than at P1, but similar changes were not observed in hyperoxic mice. The temporally and spatially specific alterations in the expressions of FGFR-3, FGFR-4, and FGF-7 in the mice exposed to hyperoxia may contribute to aberrant lung development.
authors.affiliation: Department of Pediatrics, Columbus Children's Research Institute, Columbus, Ohio 43205, USA.
authors.forename: Min Soo
authors.initials: MS
authors.lastname: Park
authors.forename: Esther
authors.initials: E
authors.lastname: Rieger-Fackeldey
authors.forename: Brandon L
authors.initials: BL
authors.lastname: Schanbacher
authors.forename: Angela C
authors.initials: AC
authors.lastname: Cook
authors.forename: John A
authors.initials: JA
authors.lastname: Bauer
authors.forename: Lynette K
authors.initials: LK
authors.lastname: Rogers
authors.forename: Thomas N
authors.initials: TN
authors.lastname: Hansen
authors.forename: Stephen E
authors.initials: SE
authors.lastname: Welty
authors.forename: Charles V
authors.initials: CV
authors.lastname: Smith
mesh_terms: D000367:Age Factors; D000375:Aging / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D004195:Disease Models, Animal; D051523:Fibroblast Growth Factor 7 / Q000235:genetics / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental; D018496:Hyperoxia / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D008168:Lung / Q000254:growth & development* / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D010100:Oxygen; D011650:Pulmonary Alveoli / Q000254:growth & development* / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D051498:Receptor, Fibroblast Growth Factor, Type 3 / Q000235:genetics / Q000378:metabolism*; D051499:Receptor, Fibroblast Growth Factor, Type 4 / Q000235:genetics / Q000378:metabolism*
chemical_list: C496454:Fgf7 protein, mouse; D012333:RNA, Messenger; D051523:Fibroblast Growth Factor 7; C496366:Fgfr3 protein, mouse; C496372:Fgfr4 protein, mouse; D051498:Receptor, Fibroblast Growth Factor, Type 3; D051499:Receptor, Fibroblast Growth Factor, Type 4; D010100:Oxygen