Syntaxin 1A is transiently expressed in fetal lung mesenchymal cells: Potential developmental roles

Bradley B. Brimhall, Kristan A. Sikorski, John Torday, Aliakbar Shahsafaei, Kathleen J. Haley, Mary E. Sunday

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Lung development is a complex process in which epithelial-mesenchymal interactions play a key role. A conserved secretory apparatus, the soluble N- ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex, is essential for exocytosis in many cell types. Syntaxins, located on the terminal plasma membrane (T-SNAREs), are a critical component of the secretosomal complex involved in vesicular docking, fusion, and exocytosis. We analyzed syntaxin 1A mRNA and protein in fetal rat lung ontogeny, demonstrating peak expression on about day 19 of embryonic development, immediately preceding type II pneumocyte differentiation. Syntaxin 1A is predominantly expressed by lipofibroblasts, which are required for bombesin- like peptide-induced surfactant phospholipid synthesis (choline uptake) by isolated type II cells. In organ cultures, anti-syntaxin 1A antibody HPC-1 blocks choline uptake both at baseline and when induced by bombesin-like peptide or dexamethasone. HPC-1 also promotes thymidine uptake in parallel in a dose-dependent fashion. These observations indicate a potential role for syntaxin 1A during fetal lung development, possibly through involvement in secretion of mesenchymal cell-derived factors that induce terminal type II cell differentiation.

Original languageEnglish (US)
Pages (from-to)L401-L411
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume277
Issue number2 21-2
DOIs
StatePublished - Aug 1999
Externally publishedYes

Keywords

  • Bombesin
  • Dexamethasone
  • Lung development
  • Monoclonal antibody
  • Surfactant phospholipids

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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