Title

Kcnq1 contributes to an adrenergic-sensitive steady-state K+ current in mouse heart

Authors

Authors

B. C. Knollmann; S. Sirenko; Q. Rong; A. N. Katchman; M. Casimiro; K. Pfeifer;S. N. Ebert

Comments

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Abbreviated Journal Title

Biochem. Biophys. Res. Commun.

Keywords

potassium channel; transgenic mouse; electrophysiology; adrenergic; heart; LANGE-NIELSEN-SYNDROME; POTASSIUM CHANNEL; VENTRICULAR MYOCYTES; TARGETED DISRUPTION; RAT-HEART; EXPRESSION; MICE; PROTEINS; SUBUNIT; KVLQT1; Biochemistry & Molecular Biology; Biophysics

Abstract

It has been suggested that Kcnel subunits are required for adrenergic regulation of Kcnq1 potassium channels. However, in adult mouse hearts, which do not express Kcne1, loss of Kcnq1 causes a Long QT phenotype during adrenergic challenge, raising the possibility that native Kcnq1 currents exist and are adrenergically regulated even in absence of Kcnel. Here, we used immunoblotting and immunohistochemical staining to show that Kcnq1 protein is present in adult mouse hearts. Voltage-clamp experiments demonstrated that Kcnq1 contributes to a steady-state outward current (I-SS) in wild-type (Kcnq1+/+) ventricular myocytes during isoproterenol stimulation, resulting in a significant 7.1% increase in Iss density (0.43 +/- 0.16 pA/pF, p < 0.05, n = 15), an effect that was absent in Kcnq1-deficient (Kcnq1(-/-)) myocytes (-0.14 +/- 0.13 pA/pF, n = 17). These results demonstrate for the first time that Kcnq1 protein is expressed in adult mouse hearts where it contributes to a beta-adrenergic-induced component of Iss that does not require co-assembly with Kcnel. (c) 2007 Elsevier Inc. All rights reserved.

Journal Title

Biochemical and Biophysical Research Communications

Volume

360

Issue/Number

1

Publication Date

1-1-2007

Document Type

Article

Language

English

First Page

212

Last Page

218

WOS Identifier

WOS:000248137400034

ISSN

0006-291X

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