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This Article Full Text Full Text (PDF) All Versions of this Article: 293/2/L429    most recent 00451.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Zscheppang, K. Articles by Dammann, C. E. L. Search for Related Content PubMed PubMed Citation Articles by Zscheppang, K. Articles by Dammann, C. E. L.

ErbB4 regulates fetal surfactant phospholipid synthesis in primary fetal rat type II cells

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

Submitted 16 November 2006 ; accepted in final form 31 May 2007

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 downregulation in fetal type II epithelial cells will downregulate 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 day 19 fetal rat lung type II cells. ErbB4 siRNA treatment inhibited erbB4 receptor protein expression, fibroblast-conditioned medium induced erbB4 phosphorylation, and fetal surfactant phospholipid synthesis. Cell proliferation, measured as thymidine incorporation, was also inhibited by erbB4 siRNA treatment. Downregulation 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.

small interfering RNA

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