Association of a functional polymorphism in the MMP7 gene promoter with susceptibility to vulnerable carotid plaque in a Han Chinese Population

被引:9
作者
Hu, Xiao-Fei [1 ]
Jin, Xiao-Ping [1 ]
Hu, Pei-Yang [2 ]
Zhu, Min
Wang, Feng [1 ]
Lin, Xian-Fang [3 ]
Li, Wei-Ling [1 ]
Ni, Hong [1 ]
Yang, Li-Hua [1 ]
机构
[1] Wenzhou Med Coll, Affiliated Hosp, Taizhou Hosp, Dept Neurol, Taizhou 317000, Zhejiang, Peoples R China
[2] Wenzhou Med Coll, Affiliated Hosp, Taizhou Hosp, Dept Gen Practice, Taizhou 317000, Zhejiang, Peoples R China
[3] Wenzhou Med Coll, Affiliated Hosp, Taizhou Hosp, Dept Ultrasound, Taizhou 317000, Zhejiang, Peoples R China
关键词
atherosclerosis; carotid; genetic polymorphism; matrix metalloproteinase-7; vulnerable plaque; MATRIX METALLOPROTEINASE-7 PROMOTER; ATHEROSCLEROTIC LESIONS; ARTERY ATHEROSCLEROSIS; APOLIPOPROTEIN-E; RISK-FACTOR; CANCER; STENOSIS; RUPTURE; ENDARTERECTOMY; INTERLEUKIN-6;
D O I
10.1515/CCLM.2011.241
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Background: Matrix metalloproteinase-7 (MMP-7) may play an important role in the development of vulnerable carotid plaque. An A-to-G transition (-181A/G) in the promoter region of MMP7 is functional in vitro by altering the transcriptional activity of the gene. The aim of this study was to investigate the association between the MMP7 -181A/G polymorphism and vulnerable carotid plaque formation. Methods: The authors enrolled 641 patients and divided them into three groups according to the carotid ultrasound examination: vulnerable plaque group (n=118), stable plaque group (n=385) and no plaque group (n=138). Traditional atherosclerosis risk factors were recorded and the MMP7 -181A/G polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism. Results: In the multinomial logistic regression analysis, compared to the no plaque group, no relationship between MMP7 -181AG+GG genotypes and stable carotid plaque was observed [odds ratio (OR) 1.50; p=0.239]. However, the frequency of AG+GG genotypes was significantly higher in the vulnerable plaque group (OR 2.74; p=0.008). Age was a risk factor for plaque formation, while statin treatment can reduce the prevalence of atherosclerotic plaque. Additionally, using binary logistic regression analysis between the stable and vulnerable plaque groups, this MMP7 polymorphism was associated with vulnerable plaque independently of other factors [OR 1.83; 95% confidence interval 1.083.11; p=0.026]. Conclusions: The MMP7 -181A/G polymorphism is associated with the development of vulnerable carotid plaques. Age is a risk factor for plaque formation, while statin therapy is associated with a decreased prevalence of carotid atheromatous plaques.
引用
收藏
页码:1735 / 1741
页数:7
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