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Am J Physiol Lung Cell Mol Physiol 286: L331-L336, 2004. First published October 17, 2003; doi:10.1152/ajplung.00334.2003
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Pulmonary surfactant secretion in briefly cultured mouse type II cells

Laurice I. Gobran and Seamus A. Rooney

Division of Perinatal Medicine, Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut 06510

Submitted 17 September 2003 ; accepted in final form 10 October 2003

There is little information on the regulation of surfactant secretion in mouse type II cells. We isolated type II cells from C57BL/6 and FVB mice, cultured them overnight, and then examined their response to known surfactant secretagogues. Secretion of phosphatidylcholine, surfactant protein (SP)-B and SP-C was stimulated by terbutaline, 5'-N-ethylcarboxyamidoadenosine (NECA), ATP, UTP, TPA, and ionomycin. Phosphatidylcholine secretion was increased approximately twofold by all agonists in both strains of mice. The response to terbutaline and NECA is the same as in rat type II cells, whereas the response to ATP, UTP, TPA, and ionomycin is considerably less. Secretion of SP-B and SP-C was increased sevenfold by terbutaline and threefold by ATP, effects similar to those in rat type II cells. The response to terbutaline was significantly decreased in type II cells from {beta}2-adrenergic receptor null mice. These data establish that briefly cultured type II cells provide a suitable model for investigation of surfactant secretion in normal and genetically altered mice.

phosphatidylcholine; surfactant protein B; surfactant protein C; exocytosis; {beta}2-adrenergic receptor null mice



Address for reprint requests and other correspondence: S. A. Rooney, Dept. of Pediatrics, Yale Univ. School of Medicine. PO Box 208064, New Haven, CT 06520-8064 (E-mail: Seamus.Rooney{at}Yale.edu).




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