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Papers In Press, published online ahead of print May 14, 2002
NIH-NHLBI-LMB, NIH, Bethesda, MD 20892
Corresponding Author: finkelt{at}nih.gov
Cell death can proceed through at least two distinct pathways. Apoptosis is an energy dependent process characterized morphologically by cell shrinkage, while oncosis is a form of cell death induced by energy depletion and initially characterized by cell swelling. We demonstrate that in HeLa cells but not in normal diploid fibroblasts, modest increases in the expression level of uncoupling protein 2 (UCP-2) leads to a rapid and dramatic fall in mitochondrial membrane potential and to a reduction of mitochondrial NADH and intracellular ATP. In HeLa cells, increased UCP-2 expression leads to a form of cell death that is not inhibited by the anti-apoptotic gene product bcl-2 and that morphologically resembles cellular oncosis. We further describe the creation of a dominant interfering mutant of UCP-2 whose expression increases resting mitochondrial membrane potential and selectively increases resistance to cell death following oncotic but not apoptotic stimuli. These results suggest that distinct genetic programs may regulate the cellular response to either apoptotic or oncotic stimuli.
J. Biol. Chem, 10.1074/jbc.M111860200
Submitted on December 12, 2001
Revised on May 14, 2002
Accepted on May 14, 2002
Regulation of cellular oncosis by uncoupling protein 2
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