title: Time courses of subcellular signal transduction and cellular apoptosis in remote viable myocardium of rat left ventricles following acute myocardial infarction: role of pharmacomodulation.
abstract: 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).
authors.affiliation: Division of Cardiology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung Hsien, Taiwan, ROC.
authors.forename: Sarah
authors.initials: S
authors.lastname: Chua
authors.forename: Li-Teh
authors.initials: LT
authors.lastname: Chang
authors.forename: Cheuk-Kwan
authors.initials: CK
authors.lastname: Sun
authors.forename: Jiunn-Jye
authors.initials: JJ
authors.lastname: Sheu
authors.forename: Fan-Yen
authors.initials: FY
authors.lastname: Lee
authors.forename: Ali A
authors.initials: AA
authors.lastname: Youssef
authors.forename: Cheng-Hsu
authors.initials: CH
authors.lastname: Yang
authors.forename: Chiung-Jen
authors.initials: CJ
authors.lastname: Wu
authors.forename: Hon-Kan
authors.initials: HK
authors.lastname: Yip