Protection of Cardiomyocytes from Acute Ischemic Injury by Protein Kinase Cepsilon Expression.
10.4070/kcj.2007.37.7.327
- Author:
Jeong Nam YOO
1
;
Soo Hoon LEE
;
Sun Ik JANG
;
Sang Ok KIM
;
Kwang Hee LEE
;
Min A PARK
;
Tae Hyung LIM
;
Jin Sook KWON
;
Myeong Chan CHO
;
Young Dae KIM
Author Information
1. Department of Internal Medicine, Joeun Gangan Hospital, Busan, Korea.
- Publication Type:Original Article
- Keywords:
Myocytes, cardiac;
Protein kinase C-epsilon;
Lentivirus;
Ischemic preconditioning
- MeSH:
Adult;
Animals;
Cell Count;
Cell Death;
Coronary Vessels;
Humans;
Ischemia;
Ischemic Preconditioning;
Lentivirus;
Ligation;
Muscle Cells;
Myocardium;
Myocytes, Cardiac*;
Protein Kinase C;
Protein Kinase C-epsilon;
Protein Kinases*;
Rats
- From:Korean Circulation Journal
2007;37(7):327-333
- CountryRepublic of Korea
- Language:Korean
-
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 theepsilonisoform has been proposed as a key factor in the signaling pathway of ischemic preconditioning. However, whether PKCepsilon expression in cardiomyocytes can offer such protection from acute ischemia has not been explored. MATERIALS AND METHODS: To demonstrate a direct effect of PKCepsilon expression, a lentiviral vector system was established. Using the lentiviral vector, PKCepsilon 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, PKCepsilon expression 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 PKCepsilon vector compared to control (11.4+/-5.3% vs 20.5+/-11.3%, p<0.01). CONCLUSION: These results provide direct evidence that PKCepsilon is a central player in protection against cell death from acute ischemia.
