Pulmonary Hypoplasia and Defective Surfactant System in FrbB4-Deleted Fetal Mice
- VernacularTitle:Pulmonary Hypoplasia and Defective Surfactant System in FrbB4-Deleted Fetal Mice
- Author:
ERDENEBULGAN Purevdorj
- Publication Type:journal article
- From:Innovation
2008;5(1):26-26
- CountryMongolia
- Language:English
-
Abstract:
common dimerization partner for other ErbB receptors. Downregulation of ErbB4 by siRNA inhibits surfactant synthesis. It is unknown how pulmonary ErbB4 knock-out affects fetal lung development. HER4h"rI transgenic mice, rescued from their lethal cardiac defect, provide a valuable tool to study the function of ErbB4 during fetal lung development. We hypothesized that the deletion of ErbB4 will affect fetal lung development. We studied this hypothesis by analyzing lung morphology and surfactant synthesis and secretion in fetal ErbB4-delcted lungs. E18 HER4hcar' lungs were significantly decreased in the thickness of the saccular septa and increased in the surface density of saccules. E17 lungs showed a delayed development of pulmonary saccules. Surfactant lipid synthesis and secretion were both reduced in E18 and E17, but were not affected in E16 HER4hc"rt lungs. Expression of surfactant proteins was affected in E18 HER4hcarl" lungs, but no significant differences in surfactant protein expression were found in El7 lungs.
In vivo deletion of ErbB4 receptor in the fetal lung impairs surfactant synthesis and secretion, as well as late fetal development, indicating a crucial role for ErbB4 in fetal lung development.
