Lack of association between four SNPs in the SLC22A3-LPAL2-LPA gene cluster and coronary artery disease in a Chinese Han population: a case control study

详细信息    查看全文

• 作者：Xiaofei Lv (1)
  Yuan Zhang (2)
  Shaoqi Rao (3)
  Fengqiong Liu (1)
  Xiaoyu Zuo (4)
  Dongfang Su (1)
  Min Wang (1)
  Min Xia (1)
  Honghui Guo (5)
  Dan Feng (4)
  Changjiang Hong (2)
  Dan Li (1)
  Wenjun Ma (6)
  Ping Ouyang (3)
  Xinrui Li (1)
  Xiang Feng (1)
  Yan Yang (1)
  Wenhua Ling (1)
  Jian Qiu (2)
  
• 关键词：Association study ; CAD ; Lp(a) ; SLC22A3 ; LPAL2 ; LPA ; SNP
• 刊名：Lipids in Health and Disease
• 出版年：2012
• 出版时间：December 2012
• 年：2012
• 卷：11
• 期：1
• 全文大小：453KB
• 参考文献：1. Tr茅gou毛t DA, K枚nig IR, Erdmann J, Munteanu A, Braund PS, Hall AS, Grosshennig A, Linsel-Nitschke P, Perret C, DeSuremain M, Meitinger T, Wright BJ, Preuss M, Balmforth AJ, Ball SG, Meisinger C, Germain C, Evans A, Arveiler D, Luc G, Ruidavets JB, Morrison C, van der Harst P, Schreiber S, Neureuther K, Sch盲fer A, Bugert P, El Mokhtari NE, Schrezenmeir J, Stark K, / et al.: Genome-wide haplotype association study identifies the SLC223A-LPL2-LPA gene cluster as a risk locus for coronary artery disease. / Nature Genet 2009, 41:283鈥?85. CrossRef
  2. Kraft HG, Menzel HJ, Hoppichler F, Vogel W, Utermann G: Changes of genetic apolipoprotein phenotypes caused by liver transplantation. Implications for apolipoprotein synthesis. / J Clin Invest 1989, 83:137鈥?42. CrossRef
  3. Erqou S, Kaptoge S, Perry PL, Di Angelantonio E, Thompson A, White IR, Marcovina SM, Collins R, Thompson SG, Danesh J, Emerging Risk Factors Collaboration: Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. / JAMA 2009, 302:412鈥?23. CrossRef
  4. Nordestgaard BG, Chapman MJ, Ray K, Bor茅n J, Andreotti F, Watts GF, Ginsberg H, Amarenco P, Catapano A, Descamps OS, Fisher E, Kovanen PT, Kuivenhoven JA, Lesnik P, Masana L, Reiner Z, Taskinen MR, Tokg枚zoglu L, Tybj忙rg-Hansen A: Lipoprotein(a) as a cardiovascular risk factor: Current status. / Eur Heart J 2010, 31:2844鈥?853. CrossRef
  5. Clarke R, Peden JF, Hopewell JC, Kyriakou T, Goel A, Heath SC, Parish S, Barlera S, Franzosi MG, Rust S, Bennett D, Silveira A, Malarstig A, Green FR, Lathrop M, Gigante B, Leander K, de Faire U, Seedorf U, Hamsten A, Collins R, Watkins H, Farrall M: Genetic variants associated with lp(a) lipoprotein level and coronary disease. / N Engl J Med 2009, 361:2518鈥?528. CrossRef
  6. Dahlen GH, Stenlund H: Lp(a) lipoprotein is a major risk factor for cardiovascular disease: Pathogenic mechanisms and clinical significance. / Clin Genet 1997, 52:272鈥?80. CrossRef
  7. Boerwinkle E, Leffert CC, Lin J, Lackner C, Chiesa G, Hobbs HH: Apolipoprotein(a) gene accounts for greater than 90% of the variation in plasma lipoprotein(a) concentrations. / J Clin Invest 1992, 90:52鈥?0. CrossRef
  8. Ober C, Nord AS, Thompson EE, Pan L, Tan Z, Cusanovich D, Sun Y, Nicolae R, Edelstein C, Schneider DH, Billstrand C, Pfaffinger D, Phillips N, Anderson RL, Philips B, Rajagopalan R, Hatsukami TS, Rieder MJ, Heagerty PJ, Nickerson DA, Abney M, Marcovina S, Jarvik GP, Scanu AM, Nicolae DL: Genome-wide association study of plasma lipoprotein(a) levels identifies multiple genes on chromosome 6q. / J Lipid Res 2009, 50:798鈥?06. CrossRef
  9. Lanktree MB, Anand SS, Yusuf S, Hegele RA: Comprehensive analysis of genomic variation in the lpa locus and its relationship to plasma lipoprotein(a) in south asians, chinese, and european caucasians. / Circ Cardiovasc Genet 2010, 3:39鈥?6. CrossRef
  10. Koch W, Hoppmann P, Erl A, Schrempf M, Schatke A, Tuerk S, Mueller JC, Schoemig A, Kastrati A: Risk polymorphisms and haplotypes identified in genome-wide association studies and their relation with myocardial infarction. / Eur Heart J 2010, 31:801.
  11. Qi L, Ma J, Qi Q, Hartiala J, Allayee H, Campos H: Genetic risk score and risk of myocardial infarction in hispanics. / Circulation 2011, 123:374鈥?80. CrossRef
  12. Sawabe M, Tanaka N, Arai T, Mieno MN, Ikeda S, Muramatsu M: Genetic polymorphisms of SLC22A3-LPL2-LPA gene cluster has direct and indirect effects on coronary atherosclerosis and coronary heart disease. / HUGO J 2009, 4:107.
  13. Shaw SY, Cheng S, Cupples LA, Larson MG, McCabe EL, Ngwa JS, Wang YA, Martin RP, Klein RJ, Hashmi B, Ajijola OA, Lau E, O鈥橠onnell CJ, Vasan RS, Cohen KS, Wang TJ: Genetic and clinical correlates of early-outgrowth colony-forming units. / Circ Cardiovasc Genet 2011, 4:296鈥?04. CrossRef
  14. Lanktree MB, Anand SS, Yusuf S, Hegele RA: Replication of genetic associations withplasma lipoprotein traits in a multiethnic sample. / J Lipid Res 2009, 50:1487鈥?496. CrossRef
  15. Qi L, Hu FB, Hu G: Genes, environment, and interactions in prevention of type 2 diabetes: A focus on physical activity and lifestyle changes. / Curr Mol Med 2008, 8:519鈥?32. CrossRef
  16. Qi L, Cho YA: Gene-environment interaction and obesity. / Nutr Rev 2008, 66:684鈥?94. CrossRef
  17. Qi Q, Workalemahu T, Zhang C, Hu FB, Qi L: Genetic variants, plasma lipoprotein(a) levels, and risk of cardiovascular morbidity and mortality among two prospective cohorts of type 2 diabetes. / Eur Heart J 2011. Epub ahead of print.
  18. Lv X, Zhang Y, Rao S, Qiu J, Wang M, Luo X, Zuo X, Su D, Feng X, Yang Y, Ouyang P, Chen Y, Li X, Xiao Y, Ling W: Joint effects of genetic variants in multiple Loci on the risk of coronary artery disease in chinese han subjects. / Circ J 2012,76(8):1987鈥?992. CrossRef
  19. Samani NJ, Deloukas P, Erdmann J, Hengstenberg C, Kuulasmaa K, McGinnis R, Schunkert H, Soranzo N, Thompson J, Tiret L, Ziegler A: Large scale association analysis of novel genetic loci for coronary artery disease. / Arterioscler Thromb Vasc Biol 2009, 29:774鈥?80. CrossRef
  20. Pask R, Rance HE, Barratt BJ, Nutland S, Smyth DJ, Sebastian M, Twells RC, Smith A, Lam AC, Smink LJ, Walker NM, Todd JA: Investigating the utility of combining phi29 whole genome amplification and highly multiplexed single nucleotide polymorphism beadarray genotyping. / BMC Biotechnol 2004, 4:15. CrossRef
  21. Lewis CM: Genetic association studies: Design, analysis and interpretation. / Brief Bioinform 2002, 3:146鈥?53. CrossRef
  22. Dupont WD, Plummer WD Jr: Power and sample size calculations for studies involving linear regression. / Control Clinical Trials 1998, 19:589鈥?01. CrossRef
  
• 作者单位：Xiaofei Lv (1)
  Yuan Zhang (2)
  Shaoqi Rao (3)
  Fengqiong Liu (1)
  Xiaoyu Zuo (4)
  Dongfang Su (1)
  Min Wang (1)
  Min Xia (1)
  Honghui Guo (5)
  Dan Feng (4)
  Changjiang Hong (2)
  Dan Li (1)
  Wenjun Ma (6)
  Ping Ouyang (3)
  Xinrui Li (1)
  Xiang Feng (1)
  Yan Yang (1)
  Wenhua Ling (1)
  Jian Qiu (2)
  
  1. Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Nutrition, School of Public Health, Sun Yat-Sen University (Northern Campus), 74 Zhongshan Road 2, Guangzhou, 510080, China
  2. Department of Cardiology, Guangzhou Region General Hospital, 111 Liuhua Road, Guangzhou, 510070, China
  3. Institute of Medical Systems Biology; Department of Medical Statistics and Epidemiology, School of Public Health, Guangdong Medical College, Dongguan, Guangdong, 523808, China
  4. Department of Medical Statistics and Epidemiology, School of Public Health, Sun Yat-Sen University (Northern Campus), 74 Zhongshan Road 2, Guangzhou, 510080, China
  5. Department of Food Science, Yingdong College of Bioengineering, Shaoguan University, Daxue Road, Shaoguan, 512005, Guangdong Province, China
  6. Department of Nutrition, Guangdong Provincial People鈥檚 Hospital, 106 Zhongshan Road 2, Guangzhou, 510080, China
  

文摘

Background Lipoprotein (a) (Lp [a]) is known being correlated with coronary artery disease (CAD). The SLC22A3-LPAL2-LPA gene cluster, relating with modulating the level of plasma Lp (a), has recently been reported to be associated with CAD in Caucasians. The purpose of this study was to verify whether this finding can be expanded to the Chinese Han population. Methods and Results Using a Chinese Han sample, which consisted of 1012 well-characterized CAD patients and 889 healthy controls, we tested the associations of four SNPs (rs2048327, rs3127599, rs7767084 and rs10755578) in the SLC22A3-LPAL2-LPA gene cluster, and their inferred haplotypes with the risk of CAD. Allelic, genotypic and haplotype association analyses all showed that the gene cluster was not associated with CAD in this Chinese Han sample. Conclusions We for the first time explored the association of the four SNPs in the SLC22A3-LPAL2-LPA gene cluster with CAD in a large Chinese Han sample. Nevertheless, this study did not reveal any significant evidence of this gene cluster to increase the risk of CAD in this population.