Alteration of the expression of ion channels, ion exchangers and Ca2+-handling proteins in ischemic cardiomyocytes

Abstract

[한글]

[영문]Myocardial infarction results in inability to supply adequate oxygen and cause damage to the cardiac muscle and has been associated with conditions of pathological stress that impair myocardial homeostasis. It has been known the effect of calcium in myocardium but there are few studies for calcium regulation of early ischemic cardiomyocytes. Early ischemia was induced in 3 to 6 hours and membrane/cytosol ratio of PKC was up-regulated in this condition. Early ischemia was suppressed the phosphorylation levels of Erk and Akt as well as anti-apoptotic proteins, Bcl-2, and induction of pro-apoptotic protein, Bax. Calcium-related gene expression in ischemic cardiomyocytes was investigated by microarray. Early ischemic condition induced reactive oxygen species (ROS), intracellular Ca2+, and Na+ overload. In early ischemic condition, the expression of Ca2+-handling protein (calsequestrin, calmodulin, and calreticulin), ion exchanger(NCX) and ion channel (RyR2), ion pump (Na+-K+-ATPase, SERCA2a and PLB) and stress markers(ANP and BNP) were significantly altered. In conclusion, early ischemic condition alters Ca2+-related gene expression in cardiomyocytes. This results indicate that early ischemia have may provide strategies to define calcium regulation