Bcl-x(L) regulates the membrane potential and volume homeostasis of mitochondria

Matthew G. Vander Heiden*, Navdeep S. Chandel, Edward K. Williamson, Paul T. Schumacker, Craig B. Thompson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1206 Scopus citations

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 languageEnglish (US)
Pages (from-to)627-637
Number of pages11
JournalCell
Volume91
Issue number5
DOIs
StatePublished - Nov 28 1997

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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