Time courses of subcellular signal transduction and cellular apoptosis in remote viable myocardium of rat left ventricles following acute myocardial infarction: Role of pharmacomodulation

Sarah Chua, Li Teh Chang, Cheuk Kwan Sun, Jiunn Jye Sheu, Fan Yen Lee, Ali A. Youssef, Cheng Hsu Yang, Chiung Jen Wu, Hon Kan Yip

Research output: Contribution to journalJournal Article peer-review

6 Scopus citations

Abstract

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).

Original languageEnglish
Pages (from-to)104-115
Number of pages12
JournalJournal of Cardiovascular Pharmacology and Therapeutics
Volume14
Issue number2
DOIs
StatePublished - 06 2009
Externally publishedYes

Keywords

  • Acute myocardial infarction
  • Cellular apoptosis
  • P38 mitogen-activated protein kinase
  • Pharmacomodulation
  • Protein kinase C epsilon

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