The small conductance K+ channel, KCNQ1: expression, function, and subunit composition in murine trachea

• Published in: The Journal of biological chemistry 2001-11, Vol.276 (45), p.42268-42275
• Main Authors: Grahammer, F, Warth, R, Barhanin, J, Bleich, M, Hug, M J
• Format: Article
• Language: English
• Subjects: Adenosine Triphosphate - pharmacology; Animals; Calcium - metabolism; Chlorides - metabolism; Cyclic AMP - physiology; Indoles - pharmacology; KCNQ Potassium Channels; KCNQ1 Potassium Channel; Mice; Mice, Inbred C57BL; Mice, Knockout; Potassium Channels - chemistry; Potassium Channels - genetics; Potassium Channels - physiology; Potassium Channels, Voltage-Gated; Protein Subunits; Trachea - chemistry
• ISSN: 0021-9258
• DOI: 10.1074/jbc.M105014200

The gene KCNQ1 encodes a K(+) channel alpha-subunit important for cardiac repolarization, formerly known as K(v)LQT1. 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 Ca(2+) 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.