Lack of evidence to support the association of polymorphisms within the TNFSF4 gene and coronary heart disease in a Chinese Han population

Cheng,Guanghui; Wang,Hui; Chen,Minzhi; Li,Li; Gong,Yaoqin; Liu,Qiji

doi:10.3892/etm.2010.188

Lack of evidence to support the association of polymorphisms within the TNFSF4 gene and coronary heart disease in a Chinese Han population

Authors:
- Guanghui Cheng
- Hui Wang
- Minzhi Chen
- Li Li
- Yaoqin Gong
- Qiji Liu
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Affiliations: Department of Medical Genetics and Key Laboratory for Experimental Teratology of the Ministry of Education, Shandong University School of Medicine, Jinan, Shandong 250012, P.R. China, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Department of Cardiology, Qilu Hospital, Shandong University, Jinan 250012, P.R. China
Published online on: December 16, 2010 https://doi.org/10.3892/etm.2010.188
Pages: 275-280

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Abstract

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 five 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.

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