Time courses of subcellular signal transduction and cellular apoptosis in remote viable myocardium of rat left ventricles following acute myocardial infarction: role of pharmacomodulation.
We tested hypothesis that acute myocardial infarction (AMI) induces cellular apoptosis and serial changes of protein kinase C epsilon (PKC-epsilon) 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-epsilon 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).
Chua
Sarah
S
Division of Cardiology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung Hsien, Taiwan, ROC.
Chang
Li-Teh
LT
Sun
Cheuk-Kwan
CK
Sheu
Jiunn-Jye
JJ
Lee
Fan-Yen
FY
Youssef
Ali A
AA
Yang
Cheng-Hsu
CH
Wu
Chiung-Jen
CJ
Yip
Hon-Kan
HK