Influences of genetic variants in interleukin-15 gene and serum interleukin-15 levels on coronary heart disease

被引:25
|
作者
Gokkusu, Cahide [2 ]
Aydin, Makbule [1 ]
Ozkok, Elif [1 ]
Tulubas, Feti [2 ]
Elitok, Ali [3 ]
Pamukcu, Burak [3 ]
Umman, Berrin [3 ]
机构
[1] Istanbul Univ, Inst Expt Med, Dept Neurosci, Istanbul, Turkey
[2] Istanbul Univ, Dept Biochem, Istanbul Fac Med, Istanbul, Turkey
[3] Istanbul Univ, Dept Cardiol, Istanbul Fac Med, Istanbul, Turkey
关键词
IL-15; Inflammation; Cororary heart disease; Polymorphism; C-REACTIVE PROTEIN; T-CELLS; INFLAMMATION; IL-15; ATHEROSCLEROSIS; ASSOCIATION; EXPRESSION; POLYMORPHISMS; ACTIVATION; MECHANISMS;
D O I
10.1016/j.cyto.2009.09.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Interleukin-15 (IL-15) is a potent proinflammatory cytokine that is now considered a key component of atherosclerosis. Proinflammatory gene polymorphisms lead to variations in the production and level of the proteins. In light of these findings, we hypothesized that variations in the gene coding for IL-15 influence the risk of coronary heart disease (CHD) by modulating the IL-15 levels. To test this hypothesis, we examined 5 single nucleotide polymorphisms (SNPs) in IL-15 gene and IL-15 levels in 102 patients with acute coronary syndrome (ACS), 102 patients with chronic ischemic stable CHD and 162 healthy control subjects. This study is the first report showing the influences of IL-15 gene variants and IL-15 levels on CHD. The five single nucleotide polymorphisms (SNPs) within the IL-15 gene, G367A, C267T, A14035T, C13687A, and A10504G were carried out by polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP). Serum IL-15 levels were significantly higher in both acute and chronic patients than in controls. Genetic variants of IL-15 gene and IL-15 levels were associated with CHID. In conclusion, our study supports the hypothesis that genetic variation in IL-15 gene and IL-15 levels influence the risk of CHID. Further studies are needed to confirm our hypothesis. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:58 / 63
页数:6
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