Activation of JNK in the remote myocardium after large myocardial infarction in rats.
A large myocardial infarction (MI) causes a chronic hemodynamic load on the uninjured remote myocardium (RM). This may lead to oxidative stress, activation of stress-induced cell signaling and increase in myocyte apoptosis. MI was produced in 6 rats (INF) while 4 rats underwent sham operation (CON). At four weeks, there was 128% increase in right ventricular hypertrophy in the hearts from INF vs. CON. Western blot analysis showed 3.8 fold increase in JNK phosphorylation within the RM from INF vs. CON, confirmed by a 4.2 fold increase in JNK kinase activity. There was a 52% increase in TBARS within the RM from INF vs. CON, suggesting increased lipid peroxidation. Furthermore, there was a twofold increase in myocyte apoptosis within the RM in INF vs. CON. We conclude that the RM from INF is associated with activation of JNK, increased oxidative stress and enhanced myocyte apoptosis.
Li
W G
WG
Department of Internal Medicine, University of Iowa, Iowa City, USA.
Zaheer
A
A
Coppey
L
L
Oskarsson
H J
HJ
D000818:Animals; D017209:Apoptosis; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism*; D004789:Enzyme Activation; D006333:Heart Failure / Q000201:enzymology; D017380:Hypertrophy, Right Ventricular; D048031:JNK Mitogen-Activated Protein Kinases; D008297:Male; D020928:Mitogen-Activated Protein Kinases; D009203:Myocardial Infarction / Q000201:enzymology* / Q000473:pathology; D009206:Myocardium / Q000201:enzymology*; D018384:Oxidative Stress; D010766:Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
D017392:Thiobarbituric Acid Reactive Substances; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases