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Activation of JNK in the remote myocardium after large myocardial infarction in rats
Abstract:
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.
Insights
Following myocardial infarction (MI), the remote myocardium (RM) experiences increased stress, leading to oxidative stress, JNK signaling activation, and myocyte apoptosis in rats. This study details these detrimental effects on heart tissue after infarction.
Area of Science:
- Cardiology
- Molecular Biology
- Pathophysiology
Background:
- Large myocardial infarction (MI) imposes chronic hemodynamic load on remote myocardium (RM).
- This stress can trigger oxidative stress, cell signaling pathways, and myocyte apoptosis.
- Understanding RM response is crucial for managing post-MI complications.
Purpose of the Study:
- To investigate the molecular and cellular changes in the remote myocardium (RM) following a large myocardial infarction (MI).
- To assess the role of JNK signaling, oxidative stress, and apoptosis in the uninjured RM after MI.
Main Methods:
- Myocardial infarction (MI) was induced in rats (INF group).
- Sham operation served as the control (CON group).
- Evaluated right ventricular hypertrophy, JNK phosphorylation and activity, TBARS levels, and myocyte apoptosis in RM at four weeks post-MI.
Main Results:
- A 128% increase in right ventricular hypertrophy was observed in INF vs. CON rats.
- JNK phosphorylation and kinase activity increased significantly (3.8-fold and 4.2-fold, respectively) in RM of INF rats.
- TBARS levels, indicating lipid peroxidation, rose by 52% in RM from INF rats.
- Myocyte apoptosis doubled in the RM of INF rats compared to CON rats.
Conclusions:
- The remote myocardium (RM) in rats after myocardial infarction (MI) exhibits significant JNK pathway activation.
- Increased oxidative stress and enhanced myocyte apoptosis are key features of the RM response to MI.
- These findings highlight the detrimental impact of infarction on remote heart tissue, suggesting potential therapeutic targets.