Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 282, Issue 4, Pages L727-L734Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00281.2001
Keywords
Bcl-XL; hypoxia; hypoxia inducible factor-1; tumor necrosis factor-alpha; nuclear factor-kappa B
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Funding
- NIGMS NIH HHS [GM-60472-02] Funding Source: Medline
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The intracellular signaling pathways that control O-2 deprivation (anoxia)-induced apoptosis have not been fully defined in lung epithelial cells. We show here that the lung epithelial cell line A549 releases cytochrome c and activates caspase-9 followed by DNA fragmentation and plasma membrane breakage in response to anoxia. The antiapoptotic protein Bcl-XL prevented the anoxia-induced cell death by inhibiting the release of cytochrome c and caspase-9 activation. A549 cells devoid of mitochondrial DNA (rhodegrees-cells) and lacking a functional electron transport chain were resistant to anoxia-induced apoptosis. A549 cells preconditioned with either hypoxia (1.5% O-2) or tumor necrosis factor-alpha, which activated the transcription factors hypoxia-inducible factor-1 or nuclear factor-kappaB, respectively, did not provide protection from anoxia-induced cell death. These results indicate that A549 cells require a functional electron transport chain and the release of cytochrome c for anoxia-induced apoptosis.
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