Plasma Levels of Interleukin 18, Interleukin 10, and Matrix Metalloproteinase-9 and -137G/C Polymorphism of Interleukin 18 Are Associated with Incidence of In-stent Restenosis After Percutaneous Coronary Intervention

被引:0
作者
Wenwei Liu
Yongsheng Liu
Hua Jiang
Xiangwu Ding
Rui Zhu
Bin Li
Yuqin Zhao
机构
[1] Hospital Affiliated to Hubei University of Arts and Science,Department of Cardiology
[2] Huazhong University of Science and Technology,Department of Cardiology, Xiangyang Hospital Affiliated to Tongji Medical College
来源
Inflammation | 2013年 / 36卷
关键词
interleukin-18; interleukin-10; matrix metalloproteinase-9; polymorphism; coronary artery disease; in-stent restenosis;
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学科分类号
摘要
This study aims to investigate the relationship between the levels of IL-18, IL-10, and MMP-9 and -137G/C polymorphism of interleukin 18 with the risk of in-stent restenosis (ISR). The study population consisted of 68 patients with ISR, 173 in non-ISR group, treated with drug-eluting stent and evaluated by coronary angiography post-procedure and at follow-up, and also 109 without angiographic evidence of coronary artery disease (CAD) which formed a reference control group (non-CAD group). The sequential plasma IL-18, IL-10, and MMP-9 levels were assessed at admission, 24 h, and 2 weeks after percutaneous coronary intervention. The -137G/C polymorphism of IL-18 was genotyped by the ligase detection reaction-polymerase chain reaction. Plasma IL-18 and MMP-9 increased significantly from admission, peaking after 24 h and fall after 2 weeks. Compared with the non-ISR group, the ISR group had higher levels of IL-18 and MMP-9, but IL-10 level was the opposite. The -137GG genotype of IL-18 was significantly higher than of the CG and CC genotypes. A significant higher frequency of -137G allele or GG genotype of IL-18 was observed in patients with ISR group compared with the non-ISR group. There is correlation between the changes of IL-18, IL-10, MMP-9, and ISR. IL-18 promoter -137G/C polymorphism influences IL-18 levels and the susceptibility to ISR, suggesting that IL-18-mediated pathways are causally involved in the process of ISR.
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页码:1129 / 1135
页数:6
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