Fgf10 deficiency is causative for lethality in a mouse model of bronchopulmonary dysplasia.

ABSTRACT: Inflammation-induced FGF10 protein deficiency is associated with bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurely born infants characterized by arrested alveolar development. So far, experimental evidence for a direct role of FGF10 in lung disease is lacking. Using the hyperoxia-induced neonatal lung injury as a mouse model of BPD, the impact of Fgf10 deficiency in Fgf10^+/- versus Fgf10^+/+ pups was investigated. In normoxia, no lethality of Fgf10^+/+ or Fgf10^+/- pups was observed. By contrast, all Fgf10^+/- pups died within 8 days of hyperoxic injury, with lethality starting at day 5, whereas Fgf10^+/+ pups were all alive. Lungs of pups from the two genotypes were collected on postnatal day 3 following no

SUBMITTER: Chao CM 

PROVIDER: S-EPMC5164852 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature