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Role of TASK2 in the control of apoptotic volume decrease in proximal kidney cells.

Sébastien L'Hoste1, Mallorie Poet, Christophe Duranton

  • 1UMR CNRS 6548, Université de Nice-Sophia Antipolis, 06108 Nice Cedex 2, France.

The Journal of Biological Chemistry
|October 20, 2007
PubMed
Summary

The TASK2 potassium channel regulates apoptotic volume decrease (AVD) and cell death in kidney proximal cells. Its absence reduces AVD and caspase activation, with BK channels partially compensating.

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Area of Science:

  • Cell Biology
  • Renal Physiology
  • Ion Channel Function

Background:

  • Apoptotic volume decrease (AVD) is a critical step in programmed cell death.
  • The TASK2 potassium channel was previously implicated in K+ efflux during regulatory volume decrease in kidney proximal cells.

Purpose of the Study:

  • To investigate the role of the TASK2 channel in regulating AVD and apoptosis.
  • To compare AVD and apoptosis in wild-type and TASK2 knock-out renal proximal tubule cells.

Main Methods:

  • Immortalized proximal convoluted tubule (PCT) cells from wild-type and TASK2 knock-out mice were used.
  • Apoptosis was induced using staurosporine, cyclosporin A, or tumor necrosis factor alpha.
  • Cell volume, K+ conductance, caspase-3, and reactive oxygen species (ROS) were monitored.

Main Results:

  • TASK2 channels mediated K+ conductance during AVD in wild-type PCT cells.
  • TASK2 knock-out cells showed a 59% reduction in AVD and caspase activation.
  • Large conductance calcium-activated (BK) channels partially compensated for TASK2 deletion in knock-out cells.
  • ROS production was essential for apoptosis, AVD, and K+ conductances in both cell types.

Conclusions:

  • TASK2 K+ channels are key mediators of apoptosis-induced AVD in wild-type proximal cells.
  • Iberiotoxin-sensitive BK channels play a compensatory role in TASK2 knock-out cells.
  • ROS production activates both TASK2 and BK channels during apoptosis.