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*
Centre National de Recherche Scientifique, Unité Propre de Recherche 420, Villejuif, France;
Institut National de la Santé et de la Recherche Médicale, Unit 459, Lille, France;
Centre Hépatobiliaire de l’Hôpital Paul Brousse, Villejuif, France; and
§
Department of Molecular Biology, Université Libre de Bruxelles, Rhode-Saint-Genèse, Belgium
Apoptosis is accompanied by major changes in ion
compartmentalization and transmembrane potentials. Thymocyte apoptosis
is characterized by an early dissipation of the mitochondrial
transmembrane potential, with transient mitochondrial swelling and a
subsequent loss of plasma membrane potential (
p)
related to the loss of cytosolic K+, cellular shrinkage,
and DNA fragmentation. Thus, a gross perturbation of
p occurs at the postmitochondrial stage of apoptosis.
Unexpectedly, we found that blockade of plasma membrane K+
channels by tetrapentylammonium (TPA), which leads to a
p collapse, can prevent the thymocyte apoptosis
induced by exposure to the glucocorticoid receptor agonist
dexamethasone, the topoisomerase inhibitor etoposide, 
-irradiation,
or ceramide. The TPA-mediated protective effect extends to all features
of apoptosis, including dissipation of the mitochondrial transmembrane
potential, loss of cytosolic K+, phosphatidylserine
exposure on the cell surface, chromatin condensation, as well as
caspase and endonuclease activation. In strict contrast, TPA is an
ineffective inhibitor when cell death is induced by the potassium
ionophore valinomycin, the specific mitochondrial benzodiazepine ligand
PK11195, or by primary caspase activation by Fas/CD95 cross-linking.
These results underline the importance of K+ channels for
the regulation of some but not all pathways leading to thymocyte
apoptosis.
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