MinireviewPlasma membrane ion channels in suicidal cell death
Section snippets
Anion channels, osmolyte transport and pH regulation
Activation of Cl− channels during apoptosis has first been observed following stimulation of CD95 in Jurkat cells [35]. Subsequently, Cl− channel activation has been described in TNFα or staurosporine induced apoptosis of various cell types [20], [36]. In Jurkat cells the same channels serve regulatory cell volume decrease following osmotic cell swelling [37]. Activation of those Cl− channels by cell swelling [37] or stimulation of CD95 [35] requires the Src-like kinase Lck56. The kinase is
K+ channels
In several cell types, apoptosis is stimulated by activation of K+ channels [40], [68] and inhibited by K+ channel blockers [69], [70] or increase of extracellular K+ concentration [70], [71], [72]. Activation of K+ channels leads to hyperpolarization of the cell membrane, which increases the electrical driving force for Cl− exit into the extracellular space. Thus, as indicated above, enhanced activity of K+ channels and Cl− channels leads to cellular loss of KCl with osmotically obliged water
Ca2+ and unselective cation channels
Jurkat lymphocyte apoptosis following CD95 triggering is paralleled by inhibition of ICRAC[114], [115], a channel involved in the activation and proliferation of a wide variety of cells [116], [117], [118], [119], [120]. Thus, in the early phase of CD95 triggering, cytosolic Ca2+ activity rather decreases in Jurkat T lymphocytes [115]. On the other hand, sustained increase of cytosolic Ca2+ activity may trigger apoptosis of a variety of nucleated cells [22], [116], [117], [121], [122] and
Conclusions
Ion channels in the plasma membrane play a decisive role in the machinery eventually leading to suicidal cell death. They influence the apoptotic signalling by modifying intracellular ion concentrations and cell volume. The role of individual channels depends on the cell type, the physiological condition, the time course and the intensity of channel activation. Much has to be learned prior to a full understanding of the complex interplay between channel activity and apoptosis signalling.
Acknowledgments
The authors acknowledge the meticulous preparation of the manuscript by Lejla Subasic. The work of the authors was supported by the Deutsche Forschungsgemeinschaft, Nr. La 315/4-3, La 315/6-1, Le 792/3-3, DFG Schwerpunkt Intrazelluläre Lebensformen La 315/11-1, and Bundesministerium für Bildung, Wissenschaft, Forschung und Technologie (Center for Interdisciplinary Clinical Research) 01 KS 9602.
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