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Activation of mitogen activated protein kinases in post-infarcted patients
Reza Akbarzadeh Najar1, Sayyed Mohammad Hossein Ghaderian, Akram Sadat Tabatabaei Panah
1Department of Medical Genetics, Faculty of Medicine, Shahid Beheshti University of Medical Sciences and Health Services, Tehran, Iran.
Abstract:
Activation of mitogen-activated protein kinases (MAPKs) signaling cascade are important pathophysiologic regulators during the development of acute myocardial infarction (AMI). In present study, we designed to monitor the activity of these MAPKs in Iranian patients with AMI comparing with controls. The degree of activation (phosphorylation) of p38 kinase, p44/42 extracellular regulated kinase, and c-Jun N-terminal kinase (JNK1/2) and their corresponding activity levels were analyzed in 258 patients with AMI and 250 normal subjects. The expression of p38α mRNA was determined. These analysis were carried out immediately and 12 h after AMI. Activity of p38 and JNK1/2 MAPKs were significantly increased in patients with AMI than controls immediately after infarction. These activities were reduced during 12 h after AMI. However, there were no statistically differences in activation and activity of p44/42 in the patients and controls. The mRNA expression of p38α was increased in the patients comparing with controls. Results of this study indicate that these MAPKs signaling pathway might be activated by AMI which signal transduction involves kinase phosphorylation and play important roles in their activity. Elevated activity of p38 and JNK1/2 MAPKs suggests that they may potentially play significant roles in AMI.
Insights
Mitogen-activated protein kinases (MAPKs) are activated during acute myocardial infarction (AMI). p38 and JNK1/2 MAPK activity increased significantly in AMI patients, suggesting their role in the condition.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Signal Transduction
Background:
- Mitogen-activated protein kinases (MAPKs) are crucial in cellular responses and disease pathogenesis.
- MAPK signaling pathways are implicated in the pathophysiology of acute myocardial infarction (AMI).
Purpose of the Study:
- To investigate the activation status and activity of key MAPKs (p38, p44/42 ERK, JNK1/2) in Iranian patients with AMI.
- To compare MAPK activation in AMI patients with healthy controls immediately and 12 hours post-infarction.
Main Methods:
- Analysis of p38, p44/42 ERK, and JNK1/2 phosphorylation and activity levels in 258 AMI patients and 250 controls.
- Quantification of p38α mRNA expression.
- Measurements performed immediately and 12 hours after AMI onset.
Main Results:
- Significantly elevated p38 and JNK1/2 MAPK activity observed in AMI patients compared to controls immediately after infarction.
- MAPK activities (p38, JNK1/2) decreased within 12 hours post-AMI.
- No significant differences in p44/42 MAPK activation between AMI patients and controls.
- Increased p38α mRNA expression in AMI patients.
Conclusions:
- MAPK signaling pathways, particularly p38 and JNK1/2, are activated during acute myocardial infarction.
- Kinase phosphorylation is involved in AMI-induced MAPK activation and signaling.
- Elevated p38 and JNK1/2 MAPK activity suggests a significant role in AMI pathogenesis.
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