Molecular cloning and functional expression of the K channel K7.1 and the regulatory subunit KCNE1 from equine myocardium.

BACKGROUND

The voltage-gated K-channel K7.1 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).

AIM

To characterize equine K7.1/KCNE1 currents and compare them to human K7.1/KCNE1 currents to determine whether K7.1/KCNE1 plays a similar role in equine and human hearts.

METHODS

mRNA encoding K7.1 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.

RESULTS

Equine K7.1/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.

CONCLUSION

The results suggest that the equine K7.1/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.