Inhibition of apoptosis by 60% oxygen: a novel pathway contributing to lung injury in neonatal rats
Autor: | Jun Li, A. Keith Tanswell, Rosetta Belcastro, Samuel Shek, Azhar Masood, Crystal Kantores, Ben-Hur Johnson, Robert P. Jankov, Adrian J A Ziino, Man Yi |
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Rok vydání: | 2011 |
Předmět: |
Pulmonary and Respiratory Medicine
medicine.medical_specialty Pathology Physiology Blotting Western Apoptosis Cell Count Lung injury Rats Sprague-Dawley Physiology (medical) Internal medicine Survivin medicine Animals Respiratory system Lung Hyperoxia Cell Death Caspase 3 business.industry Air Respiratory disease Lung Injury Cell Biology respiratory system Staurosporine medicine.disease Immunohistochemistry Rats respiratory tract diseases Oxygen Endocrinology medicine.anatomical_structure Animals Newborn Bronchopulmonary dysplasia Female medicine.symptom business Signal Transduction |
Zdroj: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 300:L319-L329 |
ISSN: | 1522-1504 1040-0605 |
DOI: | 10.1152/ajplung.00126.2010 |
Popis: | During early postnatal alveolar formation, the lung tissue of rat pups undergoes a physiological remodeling involving apoptosis of distal lung cells. Exposure of neonatal rats to severe hyperoxia (≥95% O2) both arrests lung growth and results in increased lung cell apoptosis. In contrast, exposure to moderate hyperoxia (60% O2) for 14 days does not completely arrest lung cell proliferation and is associated with parenchymal thickening. On the basis of similarities in lung architecture observed following either exposure to 60% O2, or pharmacological inhibition of physiological apoptosis, we hypothesized that exposure to 60% O2would result in an inhibition of physiological lung cell apoptosis. Consistent with this hypothesis, we observed that the parenchymal thickening induced by exposure to 60% O2was associated with decreased numbers of apoptotic cells, increased expressions of the antiapoptotic regulator Bcl-xL, and the putative antiapoptotic protein survivin, and decreased expressions of the proapoptotic cleaved caspases-3 and -7. In summary, exposure of the neonatal rat lung to moderate hyperoxia results in an inhibition of physiological apoptosis, which contributes to the parenchymal thickening observed in the resultant lung injury. |
Databáze: | OpenAIRE |
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