[Ca2+]i elevation and oxidative stress induce KCNQ1 protein translocation from the cytosol to the cell surface and increase slow delayed rectifier (IKs) in cardiac myocytes

Abstract

Background: The degree of KCNQ1/KCNE1 (IKs components) colocalization in cardiomyocytes is unclear. Results: In ventricular myocytes, KCNE1 is mainly on the cell surface, whereas KCNQ1 is mainly in the intracellular compartment. [Ca2+]i elevation or oxidative stress triggers KCNQ1 trafficking to the cell surface. Conclusion: Stress-induced KCNQ1 trafficking influences IKs amplitude. Significance: This is a novel mechanism for IKs function as a "ventricular repolarization reserve.". © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.