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Apoptosis recruits two-pore domain potassium channels used for homeostatic volume regulation

Record type: Article

Cell shrinkage is an incipient hallmark of apoptosis and is accompanied by potassium release that decreases the concentration of intracellular potassium and regulates apoptotic progression. The plasma membrane K+ channel recruited during apoptosis has not been characterized despite its importance as a potential therapeutic target. Here we provide evidence that two-pore domain K+ (K(2P)) channels underlie K+ efflux during apoptotic volume decreases (AVD) in mouse embryos. These K(2P) channels are inhibited by quinine but are not blocked by an array of pharmacological agents that antagonize other K+ channels. The K(2P) channels are uniquely suited to participate in the early phases of apoptosis because they are not modulated by common intracellular messengers such as calcium, ATP, and arachidonic acid, transmembrane voltage, or the cytoskeleton. A K+ channel with similar biophysical properties coordinates regulatory volume decreases (RVD) triggered by changing osmotic conditions. We propose that K(2P) channels are the pathway by which K+ effluxes during AVD and RVD and that apoptosis co-opts mechanisms more routinely employed for homeostatic cell volume regulation

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Citation

Trimarchi, James R., Liu, Lin, Smith, Peter J.S. and Keefe, David L. (2002) Apoptosis recruits two-pore domain potassium channels used for homeostatic volume regulation American Journal of Physiology. Cell Physiology, 282, (3), C588-C594. (doi:10.1152/ajpcell.00365.2001). (PMID:11832344).

More information

Published date: March 2002
Organisations: University of Southampton

Identifiers

Local EPrints ID: 188841
URI: http://eprints.soton.ac.uk/id/eprint/188841
ISSN: 0363-6143
PURE UUID: d9863840-5f0f-4c39-9028-02503c8cf30e
ORCID for Peter J.S. Smith: ORCID iD orcid.org/0000-0003-4400-6853

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Date deposited: 13 Jun 2011 13:04
Last modified: 18 Jul 2017 11:41

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Contributors

Author: James R. Trimarchi
Author: Lin Liu
Author: David L. Keefe

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