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Originally published In Press as doi:10.1074/jbc.M105014200 on August 29, 2001

J. Biol. Chem., Vol. 276, Issue 45, 42268-42275, November 9, 2001
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The Small Conductance K+ Channel, KCNQ1
EXPRESSION, FUNCTION, AND SUBUNIT COMPOSITION IN MURINE TRACHEA*

Florian GrahammerDagger §, Richard Warth§||, Jacques Barhanin, Markus Bleich**, and Martin J. HugDagger Dagger §§

From the Dagger  Institute of Physiology, Albert-Ludwigs-Universität, Hermann-Herder-Strabeta e 7, D-79104 Freiburg, Germany,  Institut de Pharmacologie Moléculaire et Cellulaire, CNRS, 660 route des Lucioles, Sophia Antipolis, 06560 Valbonne, France, ** Aventis Pharma Deutschland GmbH, D-65926 Frankfurt am Main, Germany, and Dagger Dagger  Institute of Physiology, Westfälische Wilhelms Universität, Robert-Koch-Strabeta e 27a, D-48149 Münster, Germany

The gene KCNQ1 encodes a K+ channel alpha -subunit important for cardiac repolarization, formerly known as KvLQT1. In large and small intestine a channel complex consisting of KCNQ1 and the beta -subunit KCNE3 (MiRP2) is known to mediate the cAMP-activated basolateral K+ current, which is essential for luminal Cl- secretion. Northern blot experiments revealed an expression of both subunits in lung tissue. However, previous reports suggested a role of KCNE1 (minK, Isk) but not KCNE3 in airway epithelial cells. Here we give evidence that KCNE1 is not detected in murine tracheal epithelial cells and that Cl- secretion by these cells is not reduced by the knock-out of the KCNE1 gene. In contrast we show that a complex consisting of KCNQ1 and KCNE3 probably forms a basolateral K+ channel in murine tracheal epithelial cells. As described for colonic epithelium, the current through KCNQ1 complexes in murine trachea is specifically inhibited by the chromanol 293B. A 293B-sensitive current was present after stimulation with forskolin and agonists that increase Ca2+ as well as after administration of the pharmacological K+ channel activator, 1-EBIO. A 293B-inhibitable current was already present under control conditions and reduced after administration of amiloride indicating a role of this K+ channel not only for Cl- secretion but also for Na+ reabsorption. We conclude that at least in mice a KCNQ1 channel complex seems to be the dominant basolateral K+ conductance in tracheal epithelial cells.

* This work was supported by the Forschungsförderung des Landes Baden-Württemberg.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

This work is dedicated to our mentor and colleague, Prof. Dr. Rainer Greger, Institute of Physiology, Albert-Ludwigs-Universität, Frieburg, Germany.

§ These authors contributed equally to this work.

|| Supported by a fellowship from the European Molecular Biology Organization (EMBO).

§§ To whom correspondence should be addressed: Physiologisches Institut Abteilung Vegetative Physiologie, Westfälische Wilhelms Universität Münster, Robert-Koch-Str. 27a, D-48149 Münster, Germany. Tel.: ++49 251-83-55327; Fax: ++49 251-83-5331; E-mail: hugma@uni-muenster.de.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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