TY - JOUR
T1 - Molecular cloning and functional expression of the K+ channel KV7.1 and the regulatory subunit KCNE1 from equine myocardium
AU - Pedersen, Philip Juul
AU - Thomsen, Kirsten B.
AU - Flak, Jon B.
AU - Tejada, Maria de los Angeles
AU - Hauser, Frank
AU - Trachsel, Dagmar Senta
AU - Buhl, Rikke
AU - Kalbfleisch, Theodore
AU - DePriest, Michael Scott
AU - MacLeod, James N.
AU - Callø, Kirstine
AU - Klærke, Dan Arne
N1 - Corrigendum to "Molecular cloning and functional expression of the K+ channel KV7.1 and the regulatory subunit KCNE1 from equine myocardium" [Res. Vet. Sci. 113 (2017) 79-86]
PY - 2017/8
Y1 - 2017/8
N2 - Background 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). Aim 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. Methods 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. Results 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. Conclusion 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.
AB - Background 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). Aim 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. Methods 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. Results 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. Conclusion 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.
KW - Cardiac electrophysiology
KW - Equine
KW - Horse
KW - K7.1
KW - KCNE1
KW - KCNQ1
UR - https://www.sciencedirect.com/science/article/pii/S0034528817312845?via%3Dihub
U2 - 10.1016/j.rvsc.2017.09.010
DO - 10.1016/j.rvsc.2017.09.010
M3 - Journal article
C2 - 28917093
AN - SCOPUS:85029361238
SN - 0034-5288
VL - 113
SP - 79
EP - 86
JO - Research in Veterinary Science
JF - Research in Veterinary Science
ER -