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Transuterine Fetal Tracheal Occlusion Model in Mice
06:31

Transuterine Fetal Tracheal Occlusion Model in Mice

Published on: February 5, 2021

Congenital diaphragmatic hernia, tracheal occlusion, thyroid transcription factor-1, and fetal pulmonary epithelial

Cheryl J Chapin1, Robert Ertsey, Jyoji Yoshizawa

  • 1Cardiovascular Research Institute, University of California, San Francisco, 94143, USA. cheri@itsa.ucsf.edu

American Journal of Physiology. Lung Cellular and Molecular Physiology
|March 15, 2005
PubMed

Insights

Congenital diaphragmatic hernia (CDH) causes underdeveloped lungs. Tracheal occlusion (TO) in CDH fetuses improved lung growth but altered surfactant and cell development, suggesting complex effects on lung maturation.

Area of Science:

  • Developmental biology
  • Pulmonary medicine
  • Neonatal research

Background:

  • Congenital diaphragmatic hernia (CDH) is a severe birth defect linked to high mortality, primarily from pulmonary hypoplasia and hypertension.
  • Experimental tracheal occlusion (TO) in animal models shows potential to improve lung growth and maturation in CDH.

Purpose of the Study:

  • To investigate the effects of CDH and TO on fetal rat lung growth and maturation.
  • To analyze the impact on distal pulmonary epithelium, including cell differentiation and surfactant production.

Main Methods:

  • CDH was induced in fetal rats using nitrofen exposure.
  • Tracheal occlusion (TO) was performed on CDH fetuses.
  • Lung wet weight, DNA content, and gene/protein expression of surfactant proteins (SP), cell markers (RTI(40), RTII(70)), and TTF-1 were analyzed.

Main Results:

  • CDH significantly decreased lung weight and DNA content.
  • CDH+TO increased lung weight but showed intermediate DNA content.
  • CDH altered expression of SP-C, TTF-1, and RTI(40); CDH+TO partially reversed these changes, improving type I cell markers but decreasing surfactant protein expression.

Conclusions:

  • Tracheal occlusion partially reverses CDH-induced pulmonary hypoplasia and restores type I cell differentiation.
  • However, CDH+TO adversely affects surfactant protein expression in type II cells.
  • These lung development alterations may be mediated by changes in thyroid transcription factor-1 (TTF-1) expression.

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