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Time Courses of Subcellular Signal Transduction and Cellular Apoptosis in Remote Viable Myocardium of Rat Left Ventricles Following Acute Myocardial Infarction: Role of Pharmacomodulation

Division of Cardiology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung

Li-Teh Chang, PhD

Division of Basic Medical Science, Department of Nursing, Meiho Institute of Technology, Ping Tung, Taiwan

Cheuk-Kwan Sun, MD, PhD

Department of General Surgery, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung

Jiunn-Jye Sheu, MD

Department of Cardiovascular Surgery Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung

Fan-Yen Lee, MD

Department of General Surgery,Surgery Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung

Ali A. Youssef, MD

Cardiology Department, Suez Canal University Hospital, Ismailia Egypt

Cheng-Hsu Yang, MD

Division of Cardiology, Surgery Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung

Chiung-Jen Wu, MD

Division of Cardiology,Surgery Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung

Hon-Kan Yip, MD

Division of Cardiology, Surgery, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiunghan.gung{at}msa.hinet.net

We tested hypothesis that acute myocardial infarction (AMI) induces cellular apoptosis and serial changes of protein kinase C epsilon (PKC-e) and p38 mitogen-activated protein kinase (p38 MAPK), and tested cardio-protective effect of losartan in this condition. The rats were assigned to group A (sacrificed on day 2), group B (sacrificed on day 5), and group C (sacrificed on day 14). Rats in each group were further randomized into the following groups: AMI (ligation of left coronary artery) without losartan (AMI-L0); AMI with losartan 20 mg/ kg/d (AMI-L1); and sham groups (L0 and L1). The PKC-e expression in membrane compartment was increased in AMI-L1 group than in other groups on day 5 and in AMI groups than in sham groups on day 14 (P < .01). Phosphorylated form of cytosolic p38 MAPK level was increased in AMI-L1 than in other groups on day 14 (P < .05). Furthermore, 14-day left ventricular ejection fraction was higher and cellular apoptosis was lower in AMI-L1 group than in AMI-L0 group (P < .0001).

Key Words: acute myocardial infarction • protein kinase C epsilon • p38 mitogen-activated protein kinase • cellular apoptosis • pharmacomodulation

This version was published on June 1, 2009

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 14, No. 2, 104-115 (2009)
DOI: 10.1177/1074248409332841


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