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Am J Physiol Lung Cell Mol Physiol (June 1, 2007). doi:10.1152/ajplung.00451.2006
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Submitted on November 16, 2006
Accepted on May 31, 2007

ErbB4 Regulates Fetal Surfactant Phospholipid Synthesis in Primary Fetal Rat Type II Cells

Katja Zscheppang1, Washa Liu2, MaryAnn V Volpe2, Heber C Nielsen2, and Christiane E. L. Dammann3*

1 Department of Pediatrics, Tufts-University and Floating Hospital for Children, Boston, Massachusetts, United States; University of Applied Sciences Lausitz, Senftenberg, Germany; Department of Pediatric Pulmonology and Neonatology, Hannover Medical School, Hannover, Germany
2 Department of Pediatrics, Tufts-University and Floating Hospital for Children, Boston, Massachusetts, United States
3 Department of Pediatrics, Tufts-University and Floating Hospital for Children, Boston, Massachusetts, United States; Department of Pediatric Pulmonology and Neonatology, Hannover Medical School, Hannover, Germany

* To whom correspondence should be addressed. E-mail: cdammann{at}tufts-nemc.org.

Insufficient fetal surfactant production leads to respiratory distress syndrome among preterm infants. Neuregulin signals the onset of fetal surfactant phospholipid synthesis through formation of erbB receptor dimers. We hypothesized that erbB4 down regulation in fetal type II epithelial cells will down regulate not only fetal surfactant phospholipid synthesis, but also affect proliferation and erbB receptor localization. We tested these hypotheses using small interfering RNA (siRNA) directed against the erbB4 gene to silence erbB4 receptor function in cultures of primary d19 fetal rat lung type II cells. ErbB4 siRNA treatment inhibited erbB4 receptor protein expression, fibroblast conditioned medium (FCM) induced erbB4 phosphorylation, and fetal surfactant phospholipid synthesis. Cell proliferation, measured as thymidine incorporation, was also inhibited by erbB4 siRNA treatment. Down regulation of erbB4 receptor protein changed erbB1 localization at baseline and after stimulation, as determined by confocal microscopy and subcellular fractionation. We conclude that erbB4 is an important receptor in the control of fetal lung type II cell maturation.




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E. Purevdorj, K. Zscheppang, H. G. Hoymann, A. Braun, D. von Mayersbach, M.-J. Brinkhaus, A. Schmiedl, and C. E. L. Dammann
ErbB4 deletion leads to changes in lung function and structure similar to bronchopulmonary dysplasia
Am J Physiol Lung Cell Mol Physiol, March 1, 2008; 294(3): L516 - L522.
[Abstract] [Full Text] [PDF]


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