Molecular cloning and functional expression of the K(+) channel KV7.1 and the regulatory subunit KCNE1 from equine myocardium.

Authors: Pedersen, Philip J and Thomsen, Kirsten B and Flak, Jon B and Tejada, Maria A and Hauser, Frank and Trachsel, Dagmar and Buhl, Rikke and Kalbfleisch, Theodore and DePriest, Michael Scott and MacLeod, James N and Calloe, Kirstine and Klaerke, Dan A

The voltage-gated K(+)-channel KV7.1 and the subunit KCNE1, encoded by the KCNQ1 and KCNE1 genes, respectively, are responsible for termination of the cardiac action potential. In humans, mutations in these genes can predispose patients to arrhythmias and sudden cardiac death (SCD).To characterize equine KV7.1/KCNE1 currents and compare them to human KV7.1/KCNE1 currents to determine whether KV7.1/KCNE1 plays a similar role in equine and human hearts.mRNA encoding KV7.1 and KCNE1 was isolated from equine hearts, sequenced, and cloned into expression vectors. The channel subunits were heterologously expressed in Xenopus laevis oocytes or CHO-K1 cells and characterized using voltage-clamp techniques.Equine KV7.1/KCNE1 expressed in CHO-K1 cells exhibited electrophysiological properties that are overall similar to the human orthologs; however, a slower deactivation was found which could result in more open channels at fast rates.The results suggest that the equine KV7.1/KCNE1 channel may be important for cardiac repolarization and this could indicate that horses are susceptible to SCD caused by mutations in KCNQ1 and KCNE1. Copyright © 2017 Elsevier Ltd. All rights reserved.

Journal: Research in veterinary science
DOI: 10.1016/j.rvsc.2017.09.010
Year: 2017

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