K2p3.1 protein is expressed as a transmural gradient across the rat left ventricular free wall.
Autor: | Jones, Sandra A., Walton, Richard D., Morton, Michael, Lancaster, Matthew K. |
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Předmět: | |
Zdroj: | Journal of Cardiovascular Electrophysiology; Mar2019, Vol. 30 Issue 3, p383-391, 9p, 4 Graphs |
Abstrakt: | Introduction: K2p3.1, also known as TASK‐1, is a twin‐pore acid‐sensitive repolarizing K+ channel, responsible for a background potassium current that significantly contributes to setting the resting membrane potential of cardiac myocytes. Inhibition of IK2p3.1 alters cardiac repolarization and is proarrhythmogenic. In this study, we have examined the expression of K2p3.1 and function of this channel in tissue and myocytes from across the left ventricular free wall. Methods and Results: Using fluorescence immunocytochemistry, the expression of K2p3.1 protein in myocytes from the subendocardial region was found to be twice (205% ± 13.5%) that found in myocytes from the subepicardial region of the left ventricle (100% ± 5.3%). The left ventricular free wall exhibited a marked transmural gradient of K2p3.1 protein expression. Western blot analysis confirmed significantly higher K2p3.1 protein expression in subendocardial tissue (156% ± 2.5%) than subepicardial tissue (100% ± 5.0%). However, there was no difference in K2p3.1 messenger RNA expression. Whole‐cell patch clamp identified IK2p3.1 current density to be significantly greater in myocytes isolated from the subendocardium (7.66 ± 0.53 pA/pF) compared with those from the subepicardium (3.47 ± 0.74 pA/pF). Conclusions: This is the first study to identify a transmural gradient of K2p3.1 in the left ventricle. This gradient has implications for understanding ventricular arrhythmogenesis under conditions of ischemia but also in response to other modulatory factors, such as adrenergic stimulation and the presence of anesthetics that inhibits or activates this channel. [ABSTRACT FROM AUTHOR] |
Databáze: | Complementary Index |
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