Protection of Cardiomyocytes from Acute Ischemic Injury by Protein Kinase Cε Expression

Abstract

Background and Objectives:Ischemic injury is the most common and important cause of myocardial damage. Over past decades, a number of studies have identified a protective mechanism known as ischemic preconditioning, which can block or delay cell death from ischemic injury. Protein kinase C (PKC), especially theeisoform has been proposed as a key factor in the signaling pathway of ischemic preconditioning. However, whether PKCe expression in cardiomyocytes can offer such protection from acute ischemia has not been explored. Materials and Methods: To demonstrate a direct effect of PKCe expression, a lentiviral vector system was established. Using the lentiviral vector, PKCe was introduced to neonatal rat ventricular myocytes (NRVM) cultured under ischemic conditions, and also to adult rat myocardium subject to left coronary artery ligation. Results:Compared to control, PKCe ex- pression in cultured NRVM under ischemia resulted in preserved cell density and morphology, and a reduction in cell death (77.6±12.8% vs 58.1±7.2%, p<0.05). In adult rats, the infarcted area after coronary artery ligation was markedly reduced in myocardium injected with PKCe vector compared to control (11.4±5.3% vs 20.5± 11.3%, p<0.01). Conclusion:These results provide direct evidence that PKCe is a central player in protection against cell death from acute ischemia. (Korean Circulation J 2007;37:327-333)