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中国北方汉族人群IL-18基因-607C/A和-137G/C多态与心肌梗死的关联性(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2011年第3期
页码:
331-335
栏目:
临床研究
出版日期:
2011-05-12

文章信息/Info

Title:
Association of interleukin-18 gene promoter polymorphisms with myocardial infarction in a Han population of northern China
作者:
张效林裴芳黄明方闫承慧康建梁振洋韩雅玲
沈阳军区总医院心内科,辽宁 沈阳 110016
Author(s):
ZHANG Xiao-lin PEI Fang HUANG Ming-fang YAN Cheng-hui KANG Jian LIANG Zhen-yang HAN Ya-ling
Department of Cardiology, Northern Hospital, Shenyang, Liaoning 110016, China
关键词:
冠状动脉疾病心肌梗死基因单核苷酸多态性
Keywords:
coronary disease myocardial infarction gene single nucleotide polymorphism
分类号:
R541.4
DOI:
-
文献标识码:
A
摘要:
目的:近年研究发现白细胞介素-18(Interleukin18,IL-18)在冠心病(CAD)的发生、发展及粥样斑块破裂的过程中起重要作用。本研究探讨IL-18基因-607C/A和-137G/C单核苷酸多态与中国北方汉族人群心肌梗死(MI)的关系。方法: 采用序列特异性引物聚合酶链反应对432例对照组和468例MI患者进行检测,分析IL-18基因-607C/A和-137G/C单核苷酸多态的基因型和等位基因分布情况。结果: IL-18基因-607C/A单核苷酸多态3种基因型(CC型,CA型和AA型)在对照组分布频率分别为20.8 %,50.9 %和28.2 %,在MI组分别为36.3 %,44.9%和18.8%,IL-18基因-607C/A多态和中国北方汉族人群MI的发生显著相关(P<0.05)。IL-18基因-137G/C单核苷酸多态三种基因型(GG型,GC型和CC型)在对照组分布频率分别为71.3 %,26.8 %和1.9 %,在MI组分别为75.2 %,23.9 % 和0.9%,IL-18基因-137G/C单核苷酸多态与中国北方汉族人群MI无相关性(P=0.133)。两组间的基因型分布皆符合Hardy-Weinberg平衡定律。Logistic回归校正性别、年龄、体质量指数、吸烟、高血压病、高脂血症、糖尿病等CAD易患因素后,IL-18基因-607C/A多态仍是MI发病的独立的危险因素(P<0.05)。IL-18基因-607C/A和-137G/C单核苷酸多态组成的CG单体型与和MI的危险性呈正相关,而AC单体型与MI的危险性呈负相关。结论: IL-18基因-607C/A多态与中国北方汉族人群中与MI的发生独立相关。
Abstract:
AIM:To investigate the association between IL-18 promoter functional polymorphisms (-607C/A and -137G/C) and myocardial infarction (MI) in a Han population of northern China. METHODS: A case-control study was conducted in 468 patients with MI and 432 controls with normal results of coronary angiograms. Genotyping was performed by sequence-specific primer-polymerase chain reaction. RESULTS: Genotype frequencies of CC, CA and AA of the IL-18 -607C/A polymorphism were, respectively, 20.83%, 50.93% and 28.24% in the controls, and 36.32%, 44.87% and 18.81% in MI patients. Genotype frequencies of GG, GC and CC of the IL-18 -137G/C polymorphism were, respectively, 71.30%, 26.85% and 1.85% in controls and 75.21%, 23.93% and 0.86% in MI patients. Significant differences were observed in the genotype and allele distribution of -607C/A polymorphism of the IL-18 gene between cases and controls (P<0.05). Logistic regression analysis with adjustments for other well-established risk factors revealed that the -607C allele carriers had a significantly increased risk of MI compared with the non-carriers (P<0.05). No relationship between -137G/C polymorphism and MI was found in this study (P=0.133). Compared with the AC haplotype, the CG haplotype was associated with reduced occurrence of MI. CONCLUSIONS: This study shows for the first time that the IL-18 gene promoter -607C/A polymorphism can be considered a genetic risk factor for MI in a Han population of northerb China. CG haplotype is associated with MI occurrence.

参考文献/References

[1]Mallat Z,Corbaz A,Scoazec A,et al.Expression of interleukin-18 in human atherosclerotic plaques and relation to plaque instability[J].Circulation,2001,104(14):1598-1603.
[2]Blankenberg S, Luc G,Ducimetiere P,et al.Interleukin-18 and the risk of coronary heart disease in European men:the Prospective Epidemiological Study of Myocardial Infarction(PRIME)[J].Circulation,2003,108(20):2453-2459.
[3]Tiret L,Godefroy T,Lubos E,et al.Genetic analysis of the interleukin-18 system highlights the role of the interleukin-18 gene in cardiovascular disease[J].Circulation,2005,112(5):643-650.
[4]Dong GP,Yu ZS,Liang L,et al.IL-18 gene promoter-137C/G and-607C/A polymorphisms in Chinese Han children with type 1 diabetes mellitus[J]. Int J Immunogenet,2007,34(2):75-79.
[5]Pawlik A,Kurzawski M,Czerny B,et al.Interleukin-18 promoter polymorphism in patients with rheumatoid arthritis[J].Tissue Antigens,2006,67(5):415-418.
[6]Reddy P.Interleukin-18:recent advances[J].Curr Opin Hemato,2004,11(6):405-410.
[7]Anderson JL,Carlquist JF.Cytokines,interleukin-18,and the genetic determinants of vascular inflammation[J].Circulation,2005,112(5):620-623.
[8]Caligiuri G,Kaveri S,Nicoletti A.When interleukin-18 conducts, the Preludio sounds the same no matter who plays[J].Arterioscler Thromb Vasc Biol,2005,25(4):655-657.
[9]Espinola-Klein C,Rupprecht HJ,Bickel C,et al.Inflammation,atherosclerotic burden and cardiovascular prognosis[J].Atherosclerosis,2007,195(2):e126-e134.
[10]Gerdes N, Sukhova GK, Libby P, et al. Expression of interleukin (IL)-18 and functional IL-18 receptor on human vascular endothelial cells, smooth muscle cells, and macrophages: implications for atherogenesis[J]. J Exp Med, 2002, 195(2):245-257.
[11]Esposito K,Pontillo A,Ciotola M,et al.Weight loss reduces interleukin-18 levels in obese women[J].J Clin Endocrinol Metab,2002,87(8):3864-3866.
[12]Esposito K, Pontillo A,Di Palo C,et al.Effect of weight loss and lifestyle changes on vascular inflammatory markers in obese women: a randomized trial[J].JAMA,2003,289(14):1799-1804.
[13]Olusi SO, Al-Awadhi A,Abraham M.Relations of serum interleukin 18 levels to serum lipid and glucose concentrations in an apparently healthy adult population[J].Horm Res, 2003, 60(1):29-33.
[14]Gracie JA,Robertson SE,McInnes IB.Interleukin-18[J].J Leukoc Biol,2003,73(2):213-224.
[15]Liu N,Sawyer SL,Mukherjee N,et al.Haplotype block structures show significant variation among populations[J].Genet Epidemiol,2004,27(4):385-400.
[16]Segat L,Milanese M,Arosio B,et al.Lack of association between Interleukin-18 gene promoter polymorphisms and onset of Alzheimer’s disease[J].Neurobiol Aging,2010,31(1):162-164.
[17]Evans J,Collins M,Jennings C,et al.The association of interleukin-18 genotype and serum levels with metabolic risk factors for cardiovascular disease[J].Eur J Endocrinol,2007,157(5):633-640.
[18]Farhat K,Hassen E, Bouzgarrou N,et al.Functional IL-18 promoter gene polymorphisms in Tunisian nasopharyngeal carcinoma patients[J].Cytokine,2008,43(2):132-137.
[19]Hiromatsu Y,Mukai T,Kaku H,et al.IL-18 gene polymorphism confers susceptibility to the development of anti-GAD65 antibody in Graves’ disease[J]. Diabet Med,2006,23(2):211-215.
[20]Lee YJ,Kang SW,Park JJ,et al.Interleukin-18 promoter polymorphisms in patients with Behcet's disease[J].Hum Immunol,2006,67(10):812-818.
[21]Doggen CJ,Bertina RM,Cats VM,et al.Fibrinogen polymorphisms are not associated with the risk of myocardial infarction[J].Br J Haematol,2000,110(4): 935-938.

备注/Memo

备注/Memo:
收稿日期:2010-06-18.基金项目:军队“十一五”计划科技攻关课题资助项目(06G021) 通讯作者:韩雅玲,主任医师,主要从事心血管病的基础、临床及介入治疗研究Email:hanyl1976@hotmail.com 作者简介:张效林,主治医师,硕士Email:xiaolindianyu75@sina.com 共同第一作者:裴芳,主治医师,博士Email:cdy060315@163.com
更新日期/Last Update: 2011-03-17