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Mitochondrial potassium channel Kv1.3 mediates Bax-induced apoptosis in lymphocytes

Ildikò Szabó1, Jürgen Bock, Heike Grassmé

  • 1Department of Biology, University of Padova, Viale G. Colombo 3, 35121 Padua, Italy.

Proceedings of the National Academy of Sciences of the United States of America
|September 27, 2008
PubMed

Insights

Mitochondrial potassium channel Kv1.3 is crucial for lymphocyte apoptosis. Bax protein inhibits Kv1.3, triggering cell death, while blocking Kv1.3 prevents apoptosis.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • The potassium channel Kv1.3 is found in the inner mitochondrial membrane of lymphocytes.
  • Its role in apoptosis, particularly in relation to mitochondrial function, is under investigation.

Purpose of the Study:

  • To investigate the role of mitochondrial Kv1.3 in lymphocyte apoptosis.
  • To determine the interaction between Bax and mitochondrial Kv1.3.

Main Methods:

  • Genetic deficiency and siRNA suppression of Kv1.3 in mouse and human cells.
  • Over-expression of Bax and its mutants.
  • Analysis of mitochondrial membrane potential, reactive oxygen species production, and cytochrome c release.
  • Incubation of isolated mitochondria with recombinant proteins and toxins.

Main Results:

  • Cells lacking Kv1.3 resisted apoptosis induced by various stimuli, including Bax over-expression.
  • Bax directly interacted with and inhibited mitochondrial Kv1.3.
  • Inhibition of Kv1.3 in isolated mitochondria led to hyperpolarization, ROS formation, cytochrome c release, and depolarization.
  • A specific mutation in Bax (K128) abrogated its effects on Kv1.3 and mitochondria.

Conclusions:

  • Mitochondrial Kv1.3 plays a significant role in mediating lymphocyte apoptosis.
  • Bax induces apoptosis, at least partly, by interacting with and inhibiting mitochondrial Kv1.3, leading to cytochrome c release and mitochondrial depolarization.

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