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Related Experiment Videos

Mitochondrial permeability transition triggers lymphocyte apoptosis

P Marchetti1, T Hirsch, N Zamzami

  • 1National Center of Scientific Research, Research Unit 420, Villejuif, France.

Journal of Immunology (Baltimore, Md. : 1950)
|December 1, 1996
PubMed
Summary

Mitochondrial permeability transition (PT) can trigger apoptosis, a programmed cell death process. The anti-apoptotic protein Bcl-2 may directly regulate PT, preventing cell death.

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • The early stage of apoptosis involves the breakdown of the inner mitochondrial transmembrane potential (Δψm).
  • Mitochondrial permeability transition (PT) is implicated in this Δψm disruption.

Purpose of the Study:

  • To investigate whether PT is sufficient to induce apoptosis or if it is a secondary event.
  • To explore the role of PT in the apoptotic cascade.

Main Methods:

  • Utilized protoporphyrin IX (PPIX) to induce PT and Δψm disruption in thymocytes and T cells.
  • Administered bongkrekic acid, a PT inhibitor, to assess its effects on PPIX-induced apoptosis.
  • Examined the impact of mRNA/protein synthesis inhibitors and Bcl-2 overexpression on PPIX-induced apoptosis.

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Main Results:

  • PPIX induced Δψm disruption, superoxide anion generation, and nuclear apoptosis, mimicking natural apoptosis.
  • Bongkrekic acid inhibited PPIX-induced Δψm disruption and all subsequent apoptotic events.
  • Inhibitors of mRNA/protein synthesis and Bcl-2 overexpression blocked PPIX-induced apoptosis, with Bcl-2 stabilizing Δψm.

Conclusions:

  • Mitochondrial PT is sufficient to trigger apoptosis.
  • The anti-apoptotic protein Bcl-2 may directly regulate PT, offering a novel therapeutic target.