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

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Korfhagen, TR; Bruno, MD; Ross, GF; Huelsman, KM; Ikegami, M; Jobe, AH; Wert, SE; Stripp, BR; Morris, RE; Glasser, SW; Bachurski, CJ; Iwamoto, HS; Whitsett, JA

Published Date

  • September 3, 1996

Published In

Volume / Issue

  • 93 / 18

Start / End Page

  • 9594 - 9599

PubMed ID

  • 8790375

Pubmed Central ID

  • 8790375

International Standard Serial Number (ISSN)

  • 0027-8424

Digital Object Identifier (DOI)

  • 10.1073/pnas.93.18.9594

Language

  • eng

Conference Location

  • United States