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. 1996 Sep 3;93(18):9594-9.
doi: 10.1073/pnas.93.18.9594.

Altered surfactant function and structure in SP-A gene targeted mice

T R Korfhagen  1 , M D Bruno, G F Ross, K M Huelsman, M Ikegami, A H Jobe, S E Wert, B R Stripp, R E Morris, S W Glasser, C J Bachurski, H S Iwamoto, J A Whitsett
Affiliations

Altered surfactant function and structure in SP-A gene targeted mice

T R Korfhagen et al. Proc Natl Acad Sci U S A. .

Abstract

The surfactant protein A (SP-A) gene was disrupted by homologous recombination in embryonic stem cells that were used to generate homozygous SP-A-deficient mice. SP-A mRNA and protein were not detectable in the lungs of SP-A(-/-) mice, and perinatal survival of SP-A(-/-) mice was not altered compared with wild-type mice. Lung morphology, surfactant proteins B-D, lung tissue, alveolar phospholipid pool sizes and composition, and lung compliance in SP-A(-/-) mice were unaltered. At the highest concentration tested, surfactant from SP-A(-/-) mice produced the same surface tension as (+/+) mice. At lower concentrations, minimum surface tensions were higher for SP-A(-/-) mice. At the ultrastructural level, type II cell morphology was the same in SP-A(+/+) and (-/-) mice. While alveolar phospholipid pool sizes were unperturbed, tubular myelin figures were decreased in the lungs of SP-A(-/-) mice. A null mutation of the murine SP-A gene interferes with the formation of tubular myelin without detectably altering postnatal survival or pulmonary function.

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