Tracheal ligation increases cell proliferation but decreases surfactant protein in fetal murine lungs in vitro.


Conference Paper

Tracheal occlusion affects both fetal lung growth and maturation. The authors used a murine in vitro whole organ culture model to investigate these effects. The authors hypothesized that tracheal ligation would increase lung growth by increasing cell proliferation and would change surfactant protein synthesis in this system. Lungs were removed from day 14 gestation murine fetuses (term, 21 days). Tracheas were ligated and explants cultured in chemically defined, serum-free media for 1, 3, 4, 5, 7, or 14 days. DNA synthesis and cell division were assessed using a 5-bromo-2'-deoxy-uridine (BrdU) incorporation assay. Surfactant proteins A and B, markers of lung maturity, were detected using immunohistochemistry. Ligated lungs showed more BrdU-labeled cells per 1,000 x field (cells/hpf) at every time point. Ligated lungs on day 1 showed 27% more cells/hpf than unligated, on day 3, 21% more, on day 5, 54% more, on day 7, 60% more, and on day 14, 123% more (P < .05). In contrast, ligated lungs showed significantly less staining for surfactant proteins A and B than did unligated lungs. The authors conclude that tracheal ligation increases cell division but decreases surfactant protein in fetal murine lungs in vitro. These data suggest that although tracheal occlusion increases lung growth, it may decrease or delay lung maturation. This model provides a powerful tool for investigating the mechanisms underlying fetal lung development and tracheal occlusion-induced pulmonary hyperplasia.

Full Text

Cited Authors

  • Bullard, KM; Sonne, J; Hawgood, S; Harrison, MR; Adzick, NS

Published Date

  • February 1997

Published In

Volume / Issue

  • 32 / 2

Start / End Page

  • 207 - 211

PubMed ID

  • 9044123

Pubmed Central ID

  • 9044123

Electronic International Standard Serial Number (EISSN)

  • 1531-5037

International Standard Serial Number (ISSN)

  • 0022-3468

Digital Object Identifier (DOI)

  • 10.1016/s0022-3468(97)90180-9