Proapoptotic BH3-only Bcl-2 family members induce cytochrome c release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity

Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):577-82. doi: 10.1073/pnas.97.2.577.

Abstract

Through direct interaction with the voltage-dependent anion channel (VDAC), proapoptotic Bcl-2 family members such as Bax and Bak induce apoptogenic mitochondrial cytochrome c release and membrane potential (Deltapsi) loss in isolated mitochondria. Using isolated mitochondria, we showed that Bid and Bik, BH3-only proteins from the Bcl-2 family, induced cytochrome c release but not Deltapsi loss. Unlike Bax/Bak, the cytochrome c release induced by Bid/Bik was Ca(2+)-independent, cyclosporin A-insensitive, and respiration-independent. Furthermore, in contrast to Bax/Bak, Bid/Bik neither interacted with VDAC nor directly affected the VDAC activity in liposomes. Consistently, Bid/Bik induced apoptosis without Deltapsi loss, whereas Bax induced apoptosis with Deltapsi loss. These findings indicated the involvement of a different mechanism in BH3-only, protein-induced apoptogenic cytochrome c release.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Apoptosis Regulatory Proteins
  • BH3 Interacting Domain Death Agonist Protein
  • Carrier Proteins / genetics
  • Carrier Proteins / pharmacology
  • Carrier Proteins / physiology
  • Cell Line
  • Cytochrome c Group / metabolism*
  • Electric Stimulation
  • Humans
  • Intracellular Membranes / drug effects
  • Intracellular Membranes / physiology
  • Ion Channels / drug effects
  • Ion Channels / metabolism
  • Male
  • Membrane Potentials / drug effects*
  • Membrane Proteins*
  • Mitochondria, Liver / drug effects*
  • Mitochondria, Liver / enzymology
  • Mitochondria, Liver / physiology
  • Mitochondrial Proteins
  • Permeability / drug effects
  • Porins / drug effects*
  • Porins / metabolism
  • Proteins / genetics
  • Proteins / pharmacology
  • Proteins / physiology
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / pharmacology
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / pharmacology*
  • Proto-Oncogene Proteins c-bcl-2 / physiology
  • Rats
  • Rats, Inbred Strains
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / physiology
  • Recombinant Proteins / pharmacology
  • Voltage-Dependent Anion Channels
  • bcl-2-Associated X Protein

Substances

  • Apoptosis Regulatory Proteins
  • BAX protein, human
  • BH3 Interacting Domain Death Agonist Protein
  • BID protein, human
  • BIK protein, human
  • Bax protein, rat
  • Bid protein, rat
  • Carrier Proteins
  • Cytochrome c Group
  • Ion Channels
  • Membrane Proteins
  • Mitochondrial Proteins
  • Porins
  • Proteins
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Recombinant Fusion Proteins
  • Recombinant Proteins
  • Voltage-Dependent Anion Channels
  • bcl-2-Associated X Protein