Abstract
Mitochondrial physiology is disrupted in either apoptosis or necrosis. Here, we report that a wide variety of apoptotic and necrotic stimuli induce progressive mitochondrial swelling and outer mitochondrial membrane rupture. Discontinuity of the outer mitochondrial membrane results in cytochrome c redistribution from the intermembrane space to the cytosol followed by subsequent inner mitochondrial membrane depolarization. The mitochondrial membrane protein Bcl-x(L) can inhibit these changes in cells treated with apoptotic stimuli. In addition, Bcl-x(L)-expressing cells adapt to growth factor withdrawal or staurosporine treatment by maintaining a decreased mitochondrial membrane potential. Bcl-x(L) expression also prevents mitochondrial swelling in response to agents that inhibit oxidative phosphorylation. These data suggest that Bcl-x(L) promotes cell survival by regulating the electrical and osmotic homeostasis of mitochondria.
Original language | English (US) |
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Pages (from-to) | 627-637 |
Number of pages | 11 |
Journal | Cell |
Volume | 91 |
Issue number | 5 |
DOIs | |
State | Published - Nov 28 1997 |
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)