ErbB receptors in fetal lung development

• Antragstellerin: Professorin Dr. Christiane Dammann
• Fachliche Zuordnung: Kinder- und Jugendmedizin
• Förderung: Förderung von 2005 bis 2012
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 15418043

Neuregulin1 helps initiate the onset of fetal surfactant synthesis via its receptors ErbB2, ErbB3, and ErbB4 in type II cells. While ErbB4 seems to play a prominent role in normal fetal surfactant synthesis, inflammation and glucocorticoids seem to lead to a prominent involvement of ErbB2, interfering with ErbB receptor control of normal lung development. Glucocorticoids and inflammation are known stimulators of fetal surfactant synthesis, but also have negative effects on alveolar development, a major pathogenetic characteristic of bronchopulmonary dyslasia (BPD). We therefore hypothesize that ErbB4 and ErbB2 signaling is involved not only in regulating fetal lung development, but also in lung injury leading to surfactant deficiency and BPD. Three specific aims are to determine the role of ErbB4 or ErbB2 on surfactant protein expression (specific aim#1), on alveolarization (specific aim#2), and on the composition and ultra- structure of alveolar septae (specific aim#3) in ErbB4 and ErbB2 mutant mice. The long term goal of this project is to help characterize the mechanisms by which ErbB receptors regulate processes in lung maturation, and by that, contributing to the development of new therapeutic strategies to more specifically enhance fetal surfactant synthesis and other critical features of lung cell maturation to reduce the individual and societal burden of acute and chronic lung disease in preterm newborns.

• DFG-Verfahren: Sachbeihilfen
• Beteiligte Person: Professor Dr. Andreas Schmiedl