Plasma membrane ion channels in suicidal cell death

Arch Biochem Biophys. 2007 Jun 15;462(2):189-94. doi: 10.1016/j.abb.2006.12.028. Epub 2007 Jan 22.

Abstract

The machinery leading to apoptosis includes altered activity of ion channels. The channels contribute to apoptotic cell shrinkage and modify intracellular ion composition. Cl(-) channels allow the exit of Cl(-), osmolytes and HCO(3)(-) leading to cell shrinkage and cytosolic acidification. K(+) exit through K(+) channels contributes to cell shrinkage and decreases intracellular K(+) concentration, which in turn favours apoptotic cell death. K(+) channel activity further determines the cell membrane potential, a driving force for Ca(2+) entry through Ca(2+) channels. Ca(2+) may enter through unselective cation channels. An increase of cytosolic Ca(2+) may stimulate several enzymes executing apoptosis. Specific ion channel blockers may either promote or counteract suicidal cell death. The present brief review addresses the role of ion channels in the regulation of suicidal cell death with special emphasis on the role of channels in CD95 induced apoptosis of lymphocytes and suicidal death of erythrocytes or eryptosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Apoptosis Regulatory Proteins / metabolism
  • Calcium Channels / physiology*
  • Cell Size
  • Cytoprotection / physiology
  • Erythrocytes / cytology*
  • Erythrocytes / metabolism*
  • Humans
  • Ion Channel Gating / physiology
  • Models, Biological
  • Oxidative Stress / physiology
  • Potassium Channels / physiology*
  • Water-Electrolyte Balance / physiology*
  • fas Receptor / metabolism*

Substances

  • Apoptosis Regulatory Proteins
  • Calcium Channels
  • Potassium Channels
  • fas Receptor