Relationship between extracellular matrix metalloproteinase inducer and clinical type of coronary heart disease
- VernacularTitle:细胞外基质金属蛋白酶诱导因子与冠心病临床类型的关系
- Author:
Junfeng ZHANG
;
Changqian WANG
;
Jin WANG
;
Jing ZHOU
;
Jun ZHOU
;
Qiang JIAO
;
Manghua XU
- Publication Type:Journal Article
- Keywords:
extracellular matrix metalloproteinase inducer;
matrix metalloproteinase;
C-reactive protein;
atherosclerosis;
coronary heart disease
- From:
Journal of Shanghai Jiaotong University(Medical Science)
2009;29(12):1431-1433
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the relationship between extracellular matrix metalloproteinase inducer (EMMPRIN), the upstream regulatory factor of matrix metalloproteinase (MMPs), and the formation of atherosclerosis and the clinical type of coronary heart disease. Methods A total of 223 patients were classified into four groups according to results of coronary angiography (CAG) and clinical data: STEMI group (65 patients with ST-segment elevation myocardial infarction), NSTE ACS group (42 patients with non-ST-segment elevation acute coronary syndrome), SAP group (75 patients with stable angina pectoris) and normal control group (41 patients of CAG-negative). The mean fluorescence intensity (MFI) of EMMPRIN on monocytes of peripheral blood (PBMCs)were examined by flow cytometry. MMP-9 in serum was measured with ELISA; high-sensitivity C-reactive protein (hs-CRP) in serum was measured with immune velocity method. Results The EMMPRIN MFI on PBMCs in SAP group, STEMI group and NSTE ACS group was higher than that in the normal control group (P<0.05 or P<0.01). The EMMPRIN MFI in STEMI group and NSTE ACS group was higher than that in SAP group (P<0.05 or P<0.01). The expression characteristic of EMMPRIN on the PBMCs was consistent with that of hs-CRP and MMP-9 in each group. The EMMPRIN MFI of the PBMCs had positive correlation with the level of MMP-9 and hs-CRP in serum (r=0.168,P<0.05;r=0.305,P<0.01). Conclusion EMMPRIN may has promotive effect on the formation of atherosclerosis and unstablility of coronary heart disease as an upstream regulatory factor of MMPs
