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Am J Physiol Lung Cell Mol Physiol 282: L727-L734, 2002; doi:10.1152/ajplung.00281.2001
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Vol. 282, Issue 4, L727-L734, April 2002

Anoxia-induced apoptosis occurs through a mitochondria-dependent pathway in lung epithelial cells

Matthew T. Santore, David S. McClintock, Vivian Y. Lee, G. R. Scott Budinger, and Navdeep S. Chandel

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60601

The intracellular signaling pathways that control O2 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 (rho °-cells) and lacking a functional electron transport chain were resistant to anoxia-induced apoptosis. A549 cells preconditioned with either hypoxia (1.5% O2) or tumor necrosis factor-alpha , which activated the transcription factors hypoxia-inducible factor-1 or nuclear factor-kappa B, 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.

Bcl-XL; hypoxia; hypoxia inducible factor-1; tumor necrosis factor-alpha ; nuclear factor-kappa B


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