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

1254 Scopus citations


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
Issue number5
StatePublished - Nov 28 1997

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


Dive into the research topics of 'Bcl-x(L) regulates the membrane potential and volume homeostasis of mitochondria'. Together they form a unique fingerprint.

Cite this