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Articles in PresS, published online ahead of print September 21, 2001
Am J Physiol Cell Physiol, 10.1152/ajpcell.00365.2001
Submitted on August 2, 2001
Accepted on September 17, 2001
1 Lab for Reproductive Medicine, Marine Biological Laboratory, Woods Hole, MA, USA; Dept of OB/GYN, Women and Infant's Hospital, Providence, RI, USA
2 BioCurrrents Research Center, Marine Biological Laboratory, Woods Hole, MA, USA
* To whom correspondence should be addressed. E-mail: jtrimarc{at}mbl.edu.
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 potassium channel recruited during apoptosis has not been characterized despite its importance as a potential therapeutic target. Here we provide evidence that two-pore domain potassium channels (K2P channels) underlie potassium efflux during apoptotic volume decreases (AVD) in mouse embryos. These K2P channels are inhibited by quinine but not blocked by an array of pharmacological agents that antagonize other potassium channels. The K2P channels are uniquely suited to participate in the early phases of apoptosis, as they are not modulated by common intracellular messengers such as calcium, ATP, arachidonic acid, transmembrane voltage or the cytoskeleton. A potassium channel with similar biophysical properties coordinates regulatory volume decreases (RVD) triggered by changing osmotic conditions. We propose that K2P channels are the pathway by which potassium effluxes during AVD and RVD and that apoptosis co-opts mechanisms more routinely employed for homeostatic cell volume regulation.
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