Apoptosis in neonatal murine lung exposed to hyperoxia

Research output: Contribution to journalArticle

Abstract

Exposure to high concentrations of oxygen in the neonatal period may impair lung growth and is a major contributing factor to the development of bronchopulmonary dysplasia. Cell death from hyperoxic injury may occur through either an apoptotic or nonapoptotic pathway, and we were interested in determining the type of cell death that occurs in the lung of neonatal mice exposed to hyperoxia. We found increased levels of Bax messenger RNA, a gene associated with apoptosis, in the lungs of neonatal mice born and raised in 92% hyperoxia. We next determined the extent of apoptosis taking place in the lungs of neonatal mice exposed to hyperoxia using terminal deoxyribonucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling in 3.5-, 4.5-, and 5.5-d-old neonatal lung. The number of apoptotic cells in peripheral lung was significantly higher in the 3.5-, 4.5-, and 5.5-d-old mice treated with oxygen compared with that in the room-air control mice. Further, the number of apoptotic cells in the lung increased with longer exposure duration. In murine lung bronchus cells exposed to hyperoxia, growth arrest occurred after 48 h of oxygen exposure. Using annexin V binding, necrotic cell death was found to be the major form of cell death in these cells after 72 h of hyperoxic exposure. We conclude that 92% hyperoxia causes significant lung injury in neonatal mice exposed to hyperoxia, and that the number of apoptotic cells in the lung increases the longer the duration of exposure. The increase in apoptosis from hyperoxic exposure during a critical period of lung development may be an important factor in the impaired lung growth and remodeling that occur in animals exposed to high oxygen concentrations. Finally, it appears that hyperoxic injured cells in neonatal lung undergo both apoptotic and nonapoptotic cell death.

Original languageEnglish (US)
Pages (from-to)150-155
Number of pages6
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Volume25
Issue number2
StatePublished - 2001

Fingerprint

Hyperoxia
Cell death
Apoptosis
Lung
Oxygen
Cells
Cell Death
DNA Nucleotidylexotransferase
Annexin A5
Biotin
Cell Count
Labeling
Animals
Genes
Growth
Messenger RNA
Bronchopulmonary Dysplasia
Air
Lung Injury
Bronchi

ASJC Scopus subject areas

  • Cell Biology
  • Pulmonary and Respiratory Medicine
  • Molecular Biology

Cite this

Apoptosis in neonatal murine lung exposed to hyperoxia. / McGrath-Morrow, Sharon A; Stahl, J.

In: American Journal of Respiratory Cell and Molecular Biology, Vol. 25, No. 2, 2001, p. 150-155.

Research output: Contribution to journalArticle

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