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

Citation
Bb. Brimhall et al., Syntaxin 1A is transiently expressed in fetal lung mesenchymal cells: potential developmental roles, AM J P-LUNG, 21(2), 1999, pp. L401-L411
Citations number
67
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
ISSN journal
10400605 → ACNP
Volume
21
Issue
2
Year of publication
1999
Pages
L401 - L411
Database
ISI
SICI code
1040-0605(199908)21:2<L401:S1ITEI>2.0.ZU;2-9
Abstract
Lung development is a complex process in which epithelial-mesenchymal inter actions play a key role. A conserved secretory apparatus, the soluble N-eth ylmaleimide-sensitive factor attachment protein receptor (SNARE) complex, i s essential for exocytosis in many cell types. Syntaxins, located on the te rminal plasma membrane (T-SNAREs), are a critical component of the secretos omal complex involved in vesicular docking, fusion, and exocytosis. We anal yzed syntaxin 1A mRNA and protein in fetal rat lung ontogeny, demonstrating peak expression on about day 19 of embryonic development, immediately prec eding type II pneumocyte differentiation. Syntaxin 1A is predominantly expr essed by lipofibroblasts, which are required for bombesin-like peptide-indu ced surfactant phospholipid synthesis (choline uptake) by isolated type II cells. In organ cultures, anti-syntaxin 1A antibody HPC-1 blocks choline up take both at baseline and when induced by bombesin-like peptide or dexameth asone. HPC-1 also promotes thymidine uptake in parallel in a dose-dependent fashion. These observations indicate a potential role for syntaxin 1A duri ng fetal lung development, possibly through involvement in secretion of mes enchymal cell-derived factors that induce terminal type II cell differentia tion.