| First Author | Hokuto I | Year | 2004 |
| Journal | Am J Physiol Lung Cell Mol Physiol | Volume | 286 |
| Issue | 3 | Pages | L580-7 |
| PubMed ID | 14617521 | Mgi Jnum | J:133989 |
| Mgi Id | MGI:3784746 | Doi | 10.1152/ajplung.00278.2003 |
| Citation | Hokuto I, et al. (2004) FGF signaling is required for pulmonary homeostasis following hyperoxia. Am J Physiol Lung Cell Mol Physiol 286(3):L580-7 |
| abstractText | To assess the role of fibroblast growth factor (FGF) signaling in pulmonary function in the postnatal period, we generated transgenic mice in which a soluble FGF receptor (FGFR-HFc) was conditionally expressed in respiratory epithelial cells of the mouse lung, thereby inhibiting FGF activity. Although FGFR-HFc did not alter postnatal lung morphogenesis, male FGFR-HFc transgenic mice were more susceptible to hyperoxia and failed to recover when ambient oxygen concentrations were normalized. Inflammation, alveolar-capillary leak, and mortality were increased following exposure to 95% Fi(O(2)). Expression of surfactant protein (SP)-A and SP-B were significantly decreased in association with decreased immunostaining for thyroid transcription factor-1. FGF signaling is required for maintenance of surfactant homeostasis and lung function during hyperoxia in vivo, mediated, at least in part, by its role in the maintenance of SP-B expression. |
