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Am J Physiol Lung Cell Mol Physiol 281: L887-L894, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 4, L887-L894, October 2001

Augmented K+ currents and mitochondrial membrane depolarization in pulmonary artery myocyte apoptosis

Stefanie Krick, Oleksandr Platoshyn, Sharon S. McDaniel, Lewis J. Rubin, and Jason X.-J. Yuan

Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California School of Medicine, San Diego, California 92103

The balance between apoptosis and proliferation in pulmonary artery smooth muscle cells (PASMCs) is important in maintaining normal pulmonary vascular structure. Activity of voltage-gated K+ (KV) channels has been demonstrated to regulate cell apoptosis and proliferation. Treatment of PASMCs with staurosporine (ST) induced apoptosis in PASMCs, augmented KV current [IK(V)], and induced mitochondrial membrane depolarization. High K+ (40 mM) negligibly affected the ST-induced mitochondrial membrane depolarization but inhibited the ST-induced IK(V) increase and apoptosis. Blockade of KV channels with 4-aminopyridine diminished IK(V) and markedly decreased the ST-mediated apoptosis. Furthermore, the ST-induced apoptosis was preceded by the increase in IK(V). These results indicate that ST induces PASMC apoptosis by activation of plasmalemmal KV channels and mitochondrial membrane depolarization. The increased IK(V) would result in an apoptotic volume decrease due to a loss of cytosolic K+ and induce apoptosis. The mitochondrial membrane depolarization would cause cytochrome c release, activate the cytosolic caspases, and induce apoptosis. Inhibition of KV channels would thus attenuate PASMC apoptosis.

apoptosis; voltage-gated potassium channels; potassium loss; caspases; mitochondrial membrane potential depolarization


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