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[The role of activator protein-1 in unstable coronary atherosclerotic changes]
Gui-Hua Miao1, Li-Xia Yang, Feng Qi
1Department of Cardiology, Kunming General Hospital of Chengdu Military Command, Kunming 650032, China.
Insights
Activator protein-1 (AP-1) levels are significantly elevated in patients with coronary heart disease (CHD). Higher AP-1 levels correlate with more severe coronary atherosclerotic changes and plaque instability, suggesting AP-1 as a predictor of disease progression.
Area of Science:
- Molecular biology
- Cardiovascular research
- Biochemistry
Context:
- Coronary heart disease (CHD) involves atherosclerotic plaque development.
- The role of specific transcription factors, like activator protein-1 (AP-1), in CHD pathogenesis is not fully understood.
- Investigating AP-1's involvement may reveal new insights into plaque stabilization and progression.
Purpose:
- To examine the relationship between activator protein-1 (AP-1) and coronary atherosclerotic changes.
- To determine if AP-1 plays a role in the stabilization of atherosclerotic plaques in patients with CHD.
- To assess AP-1 levels in relation to different stages and severities of coronary artery disease.
Summary:
- This study measured Phospho-c-Jun, a component of AP-1, in 142 patients (107 with CHD, 35 controls) using ELISA.
- AP-1 levels were significantly higher in CHD patients compared to controls and increased with disease severity (ACS vs. SAP, type C vs. A, severe vs. light stenosis).
- Results indicate a strong correlation between elevated AP-1 and advanced coronary atherosclerosis.
Impact:
- Findings suggest a significant association between AP-1 and the progression of coronary atherosclerosis.
- AP-1 may serve as a potential biomarker for predicting the progression and stability of atherosclerotic plaques.
- This research could inform future therapeutic strategies targeting AP-1 in cardiovascular disease management.
Objective:
To investigate the relation between activator protein-1 (AP-1) and coronary atherosclerotic changes and the potential role of AP-1 in the stabilization of atherosclerotic plaques in patients with coronary heart disease (CHD).
Method:
142 patients were included in this study and divided into CHD group (107) and control group (35) according to coronary angiography (CAG). The CHD group was further divided into a stable angina pectoris (SAP) group (32) and an acute coronary syndrome (ACS) group (75) according to the clinical manifestations. In addition, the CHD group was divided into A type group, B type group and C type group according to the standard of ACC/AHA coronary change in 1988. Meanwhile, the CHD group was further divided into light stenosis group, moderate stenosis group and severe stenosis group according to the degree of coronary lesion. The lysate of cells was obtained through lysis of the leucocytes from peripheral blood with cell lysis buffer. The amount of Phospho-c-Jun in lysate was measured with enzyme-linked immunosorbent assay (ELISA). The results were demonstrated with absorbance, which reflects the amount of AP-1.
Results:
The main coronary changes in the SAP group were A type (68.7%) and the changes were mainly of light degree (53.1%); the main coronary changes in the ACS group were B type (52.0%) or C type (37.3%) and the changes were mainly of heavy degree (66.7%). The absorbance of Phospho-c-Jun in CHD group was significantly higher than that in the control subjects (1.43 +/- 0.33 vs 0.71 +/- 0.13, P < 0.001). The absorbance of Phospho-c-Jun in the ACS group was significantly higher than that in the SAP group (1.56 +/- 0.28 vs 1.14 +/- 0.25, P < 0.001). The absorbance of Phospho-c-Jun increased gradually from A type group to C type group (1.18 +/- 0.27 vs 1.42 +/- 0.26 vs 1.71 +/- 0.27, P < 0.001) and from light stenosis group to severe stenosis group (1.09 +/- 0.20 vs 1.37 +/- 0. 26 vs 1.60 +/- 0.29, P < 0.001).
Conclusion:
There is a significant relationship between AP-1 and coronary atherosclerotic changes. AP-1 may be a factor that can predict coronary arteriosclerotic progression and stability of the plaque.
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