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Programmed cell death contributes to postnatal lung development

J C Schittny1, V Djonov, A Fine

  • 1Institute of Anatomy, University of Bern, Bern, Switzerland. schittny@ana.unibe.ch

American Journal of Respiratory Cell and Molecular Biology
|June 25, 1998
PubMed
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Programmed cell death significantly increases during rat lung maturation, specifically targeting fibroblasts and type II epithelial cells. This process is crucial for thinning alveolar septa and developing the lung

Area of Science:

  • Pulmonary Biology
  • Developmental Biology
  • Cell Biology

Background:

  • Lung structural maturation, including alveolar septa and microvasculature, occurs primarily in the third postnatal week in rats.
  • Programmed cell death (apoptosis) is a potential mechanism for tissue remodeling during development.

Purpose of the Study:

  • To investigate the role of programmed cell death in the structural maturation of the rat lung.
  • To identify the cell types undergoing programmed cell death during lung development.

Main Methods:

  • Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay to detect DNA fragmentation.
  • Double-labeling with antibodies for epithelial cells (E11, MNF-116) and TUNEL.
  • Electron microscopy for detailed morphological analysis.

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Main Results:

  • An eight-fold increase in programmed cell death was observed around the third postnatal week.
  • Fibroblasts and type II epithelial cells were the primary cell types undergoing programmed cell death.
  • DNA fragmentation (TUNEL-positive) was detected in both cell types, but apoptotic bodies were exclusively found in fibroblasts.

Conclusions:

  • Programmed cell death plays a vital role in rat lung maturation by reducing fibroblast and type II epithelial cell populations.
  • Fibroblasts are cleared by neighboring fibroblasts, while type II epithelial cells may be cleared by alveolar macrophages.