Lack of evidence to support the association of polymorphisms within the TNFSF4 gene and coronary heart disease in a Chinese Han population
Lack of evidence to support the association of polymorphisms within the TNFSF4 gene and coronary heart disease in a Chinese Han population
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DOI：
10.3892/etm.2010.188
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发表时间：
2011-03-01
影响因子：
2.7
通讯作者：
Liu, Qiji
中科院分区：
文献类型：
--
作者：
Cheng, Guanghui;Wang, Hui;Liu, Qiji
冠心病是一种遗传和环境因素相互作用的复杂疾病。越来越多的证据表明，OX 40配体（OX 40 L），又称肿瘤坏死因子超家族成员4（TNFSF 4），在动脉粥样硬化的发病机制中起着关键作用。然而，在不同人群中的报告不一致，需要进一步的研究来澄清这个问题。一个基于基因的关联研究进行了使用五个单核苷酸多态性（SNPs）在以前的研究报告。采用聚合酶链反应-限制性片段长度多态性方法对547例冠心病患者和601例健康对照者进行5个SNP（rs 1234314、rs 45454293、rs3850641、rs 1234313和rs3861950）的基因分型。使用TaqMan SNP基因分型方法在另外512例病例和520例对照中进一步分型rs 1234314、rs3850641和rs3861950。研究了活SNP与CHD严重程度之间的可能关系。结果显示TNFSF 4基因多态性与CHD之间无显著相关性。此外，基因型和等位基因频率的分层分析显示，TNFSF 4多态性和CHD之间没有关联，在任何性别。最后，TNFSF 4多态性与CHD严重程度之间没有显著相关性。这些发现不支持TNFSF 4基因在中国汉族人群CHD发病机制中的作用。
Coronary heart disease (CHD) is a complex disorder resulting from the interaction of a number of genetic and environmental factors. Increasing evidence has shown that OX40 ligand (OX40L), also known as tumor necrosis factor superfamily member 4 (TNFSF4), plays a key role in the pathogenesis of atherosclerosis. However, there have been inconsistent reports in various populations, and further studies are required to clarify this issue. A gene-based association study was conducted using five single-nucleotide polymorphisms (SNPs) reported in previous studies. The five SNPs (rs1234314, rs45454293, rs3850641, rs1234313 and rs3861950) were genotyped in 547 unrelated CHD patients and 601 healthy controls in a case-control study using polymerase chain reaction and restriction fragment length polymorphism. rs1234314, rs3850641 and rs3861950 were further genotyped in an additional 512 cases and 520 controls using the TaqMan SNP genotyping method. A possible relationship between the live SNPs and the severity of CHD was investigated. The results revealed no significant association between the TNFSF4 polymorphism and CHD. In addition, the stratified analysis of genotypic and allelic frequencies showed no association between the TNFSF4 polymorphism and CHD in either gender. Finally, no significant correlation between the TNFSF4 polymorphism and CHD severity was detected. These findings do not support a role of the TNFSF4 gene in CHD pathogenesis in the Chinese Han population.