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Volume-sensitive chloride channels (ICl,vol) mediate doxorubicin-induced apoptosis through apoptotic volume decrease

Alexandra d'Anglemont de Tassigny1, Rachid Souktani, Patrick Henry

  • 1Laboratoire de Pharmacologie, Faculté de Médecine de Créteil, Université Paris XII, France and Laboratoire de Pharmacologie, INSERM E00.01, Faculté de Médecine Paris-Sud, 94270 Le Kremlin-Bicêtre, France.

Fundamental & Clinical Pharmacology
|October 16, 2004
PubMed
Summary

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Volume-sensitive chloride channels (I(Cl,vol)) drive apoptotic volume decrease (AVD) and cell death in cardiomyocytes treated with doxorubicin. Inhibiting these channels prevents doxorubicin-induced AVD and apoptosis, highlighting their critical role.

Area of Science:

  • Cardiology
  • Cell Biology
  • Molecular Biology

Background:

  • Apoptosis, or programmed cell death, involves early cell volume changes known as apoptotic volume decrease (AVD).
  • Volume-sensitive chloride channels (I(Cl,vol)) are critical regulators of cell volume.
  • The precise role of I(Cl,vol) in doxorubicin-induced apoptosis in cardiomyocytes remains to be fully elucidated.

Purpose of the Study:

  • To investigate the involvement of I(Cl,vol) and AVD in doxorubicin-induced apoptotic cell death in adult rabbit ventricular cardiomyocytes.
  • To determine if I(Cl,vol) activation is a key mechanism in doxorubicin-induced AVD and apoptosis.

Main Methods:

  • Adult rabbit ventricular cardiomyocytes were exposed to doxorubicin.
  • Cell volume changes (AVD), apoptosis markers (annexin V, caspase-3 activity), and ion channel activity (I(Cl,vol)) were measured using patch clamp electrophysiology.

Related Experiment Videos

  • The effects of I(Cl,vol) inhibitors (NPPB, IAA-94) and C(2)-ceramide were assessed.

    • Main Results:

    • Doxorubicin induced significant cell shrinkage (AVD) and increased early apoptosis markers.
    • Doxorubicin activated a chloride current consistent with I(Cl,vol).
    • Inhibiting I(Cl,vol) with NPPB or IAA-94 abolished doxorubicin-induced AVD and apoptosis, a finding confirmed with C(2)-ceramide.

    Conclusions:

    • Activation of I(Cl,vol) plays a significant role in the mechanism of doxorubicin-induced cell shrinkage (AVD) and apoptosis in adult cardiomyocytes.
    • I(Cl,vol) is a key mediator of AVD and subsequent apoptosis induced by agents like doxorubicin and C(2)-ceramide.