The associations between endothelial lipase 584C/T polymorphism and HDL-C level and coronary heart disease susceptibility: a meta-analysis

Lipids in Health and Disease

Ganwei Shi²  Weijin Weng²  Bifeng Zhang³  Zhiying Huang¹  Gaojun Cai² 

[1] Department of Pediatrics, NO.2 Hospital of Changzhou, Changzhou, Jiangsu, China;Department of Cardiology, Wujin Hospital Affiliated to Jiangsu University, Changzhou, Jiangsu Province, China;Department of Medicine, University of Chicago, Chicago, Illinois, USA

关键词: Meta-analysis;    Coronary heart disease;    Polymorphism;    High density lipoprotein cholesterol;    Endothelial lipase;   

Others  :  828370
DOI  :  10.1186/1476-511X-13-85

 received in 2014-03-15, accepted in 2014-05-04,  发布年份 2014

【 摘 要 】

Background

Studies had investigated the relationships between endothelial lipase (EL) 584C/T polymorphism and high density lipoprotein cholesterol (HDL-C) level and coronary heart disease (CHD), but the results were controversial. To investigate a more authentic associations between EL 584C/T polymorphism and HDL-C level, and the risk of CHD, we performed this meta-analysis.

Methods

We searched electric databases for all articles on the associations between EL 584C/T polymorphism and HDL-C level, and CHD risk. Odds ratios (ORs) with 95% confidence interval (CI) were used to evaluate the strength of the association between the EL 584C/T polymorphism and the CHD susceptibility. The pooled standardized mean difference (SMD) with 95% CI was used for the meta-analysis of EL 584C/T polymorphism and HDL-C level. Begg’s funnel plots and Egger’s test were used to examine the publication bias.

Results

For CHD association, the pooled OR was 0.829 (95% CI: 0.701-0.980, P = 0.028) for the dominant model and 0.882 (95% CI: 0.779-0.999, P = 0.049) for the allelic model. By meta-regression analysis, we found that only total sample size could influence the initial heterogeneity. When the subgroup analysis was carried out, we found that the protective effect only existed in the subgroups of relatively small sample size. Sensitivity analyses indicated that Tang’s study influenced the overall results significantly. We calculated the pooled ORs again after excluding Tang’s study and found the association between EL 584C/T polymorphism and the risk of CHD was not significant for any genetic model. For HDL-C level association, the carriers of 584 T allele had a higher HDL-C level than the non-carriers. The pooled SMD was 0.399 (95% CI: 0.094-0.704, P = 0.010). When the studies were stratified by ethnicity and total sample size, the positive effects existed in the Caucasians and in subgroups of larger sample size. No significant publication bias was found in the present meta-analysis.

Conclusions

The results of the present meta-analysis suggest that the carriers of EL 584 T allele have a higher HDL-C level in Caucasian populations. Whereas, it might not be a protective factor for CHD.

【 授权许可】

   
2014 Cai et al.; licensee BioMed Central Ltd.

【 参考文献 】

• [1]Mensah GA, Brown DW: An overview of cardiovascular disease burden in the United States. Health Affairs 2007, 26:38-48.
• [2]Zhou YF, Zhang J, Li ZX, Miao JL, Yin QX, Li JJ, Zhang XY, Li YY, Luo HL: Association of liver X receptor α (LXRα) gene polymorphism and coronary heart disease, serum lipids and glucose levels. Lipids Health Dis 2014, 13:34. BioMed Central Full Text
• [3]Ji YN, Wang Q, Zhan P: Intercellular adhesion molecule 1 gene K469E polymorphism is associated with coronary heart disease risk: a meta-analysis involving 12 studies. Mol Biol Rep 2012, 39:6043-6048.
• [4]Wang J, Zou L, Song Z, Lang X, Huang S, Lu F, Han L, Xu Z: Meta-analysis of RAGE gene polymorphism and coronary heart disease risk. PLoS One 2012, 7:e50790.
• [5]Cao B, Ye YZ, Rui J, Li MQ, Wang W, Wei LY, Jiao GQ: A single-nucleotide polymorphism in the proximal promoter region of the apolipoprotein M gene is associated with dyslipidaemia but not increased coronary artery diseases in Chinese populations. Lipids Health Dis 2013, 12:184. BioMed Central Full Text
• [6]Hirata K, Dichek HL, Cioffi JA, Choi SY, Leeper NJ, Quintana L, Kronmal GS, Cooper AD, Quertermous T: Cloning of a unique lipase from endothelial cells extends the lipase gene family. Biol Chem 1999, 274:14170-14175.
• [7]Jaye M, Lynch KJ, Krawiec J, Marchadier D, Maugeais C, Doan K, South V, Amin D, Perrone M, Rader DJ: A novel endothelial-derived lipase that modulates HDL metabolism. Nat Genet 1999, 21:424-428.
• [8]Yasuda T, Hirata K, Ishida T, Kojima Y, Tanaka H, Okada T, Quertermous T, Yokoyama M: Endothelial lipase is increased by inflammation and promotes LDL uptake in macrophages. J Atheroscler Thromb 2007, 14:192-201.
• [9]DeLemos AS, Wolfe ML, Long CJ, Sivapackianathan R, Rader DJ: Identification of genetic variants in endothelial lipase in persons with elevated high-density lipoprotein cholesterol. Circulation 2002, 106:1321-1326.
• [10]Paradis ME, Couture P, Bosse Y: The T111I missense mutation of the endothelial lipase gene modulates the relationship between dietary fat intake and the HDL profile in women. J Lipid Res 2003, 44:1902-1908.
• [11]Mank-Seymour AR, Durham KL, Thompson JF, Seymour AB, Milos PM: Association between single-nucleotide polymorphisms in the endothelial lipase (LIPG) gene and high-density lipoprotein cholesterol levels. Biochim Biophys Acta 2004, 16361:40-46.
• [12]Tang NP, Wang LS, Yang L, Zhou B, Gu HJ, Sun QM, Cong RH, Zhu HJ, Wang B: Protective effect of an endothelial lipase gene variant on coronary artery disease in a Chinese population. J Lipid Res 2008, 49:369-375.
• [13]Shimizu M, Kanazawa K, Hirata K, Ishida T, Hiraoka E, Matsuda Y, Iwai C, Miyamoto Y, Hashimoto M, Kajiya T, Akita H, Yokoyama M: Endothelial lipase gene polymorphism is associated with acute myocardial infarction, independently of high-density lipoprotein-cholesterol levels. Circ J 2007, 71:842-846.
• [14]Jensen MK, Rimm EB, Mukamal KJ, Edmondson AC, Rader DJ, Vogel U, Tjonneland A, Sorensen TI, Schmidt EB, Overvad K: The T111I variant in the endothelial lipase gene and risk of coronary heart disease in three independent populations. Eur Heart J 2009, 30:1584-1589.
• [15]Cai GJ, He GP, Qi CP: Association between endothelial lipase 584C/T gene polymorphism and acute coronary syndrome and lipids. Chin Heart J 2012, 2012(24):708-711.
• [16]Vergeer M, Cohn DM, Boekholdt SM, Sandhu MS, Prins HM, Ricketts SL, Wareham NJ, Kastelein JJ, Khaw KT, Kamphuisen PW, Dallinga-Thie GM: Lack of association between common genetic variation in endothelial lipase (LIPG) and the risk for CAD and DVT. Atherosclerosis 2010, 211:558-564.
• [17]Zhu JC, Jin GD, Jin CY, Xu G: Association of endothelial lipase gene Thr111Ile and Gly26Ser polymorphism with lipoprotein in patients with coronary heart disease. Chin J Pathophysiol 2009, 23:1684-1687.
• [18]Yamakawa-Kobayashi K, Yanagi H, Endo K, Arinami T, Hamaguchi H: Relationship between serum HDL-C levels and common genetic variants of the endothelial lipase gene in Japanese school-aged children. Hum Genet 2003, 113:311-315.
• [19]Hutter CM, Austin MA, Farin FM, Viernes HM, Edwards KL, Leonetti DL, McNeely MJ, Fujimoto WY: Association of endothelial lipase gene (LIPG) haplotypes with high-density lipoprotein cholesterol subfractions and apolipoprotein AI plasma levels in Japanese Americans. Atherosclerosis 2006, 185:78-86.
• [20]Liu WY, Yin RX, Zhang L, Cao XL, Miao L, Wu DF, Aung LH, Hu XJ, Lin WX, Yang DZ: Association of the LIPG 584C > T polymorphism and serum lipid levels in the Guangxi Bai Ku Yao and Han populations. Lipids Health Dis 2010, 9:110. BioMed Central Full Text
• [21]Halverstadt A, Phares DA, Ferrell RE, Wilund KR, Goldberg AP, Hagberg JM: High-density lipoprotein-cholesterol, its subfractions, and responses to exercise training are dependent on endothelial lipase genotype. Metabolism 2003, 52:1505-1511.
• [22]Moher D, Liberati A, Tetzlaff J, Altman DG, PRISMA group: Perferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. Ann Intern Med 2009, 151:264-269.
• [23]DerSimonian R, Kacker R: Random-effects model for meta-analysis of clinical trials: an update. Contemp Clin Trials 2007, 28:105-114.
• [24]Cai GJ, He GP: Endothelial lipase and cardiovascular disease. Chin Heart J 2011, 23:417-419.
• [25]Willer CJ, Sanna S, Jackson AU, Scuteri A, Bonnycastle LL, Clarke R, Heath SC, Timpson NJ, Najjar SS, Stringham HM, Strait J, Duren WL, Maschio A, Busonero F, Mulas A, Albai G, Swift AJ, Morken MA, Narisu N, Bennett D, Parish S, Shen H, Galan P, Meneton P, Hercberg S, Zelenika D, Chen WM, Li Y, Scott LJ, Scheet PA, et al.: Newly identified loci that influence lipid concentrations and risk of coronary artery disease. Nat Genet 2008, 40:161-169.
• [26]Cai G, He G, Qi C: The association between endothelial lipase -384A/C gene polymorphism and acute coronary syndrome in a Chinese population. Mol Biol Rep 2012, 39:9879-9884.
• [27]Cai GJ, He GP, Qi CP: Association of endothelial lipase -384A/C gene polymorphism with acute coronary syndrome and blood lipids in Chinese elderly. Chin J Mult Organ Dis Elder 2012, 2012(11):821-824.
• [28]Tjonneland A, Olsen A, Boll K, Stripp C, Christensen J, Engholm G, Overvad K: Study design, exposure variables, and socioeconomic determinants of participation in Diet, Cancer and Health: a population-based prospective cohort study of 57,053 men and women in Denmark. Scand J Public Health 2007, 35:432-441.
• [29]Colditz GA, Manson JE, Hankinson SE: The Nurses' Health Study: 20-year contribution to the understanding of health among women. J Womens Health 1997, 6:49-62.
• [30]Rimm EB, Giovannucci EL, Stampfer MJ, Colditz GA, Litin LB, Willett WC: Reproducibility and validity of an expanded self-administered semiquantitative food frequency questionnaire among male health professionals. Am J Epidemiol 1992, 135:1114-11126.
• [31]Tanaka H, Ishida T, Johnston TP, Yasuda T, Ueyama T, Kojima Y, Kundu RK, Quertermous T, Ishikawa Y, Hirata K: Role of endothelial lipase in plasma HDL levels in a murine model of hypertriglyceridemia. J Atheroscler Thromb 2009, 16:327-338.
• [32]Ishida T, Choi S, Kundu RK, Hirata K, Rubin EM, Cooper AD, Quertermous T: Endothelial lipase is a major determinant of HDL level. J Clin Invest 2003, 111:347-355.
• [33]Ma K, Cilingiroglu M, Otvos JD, Ballantyne CM, Marian AJ, Chan L: Endothelial lipase is a major genetic determinant for high-density lipoprotein concentration, structure, and metabolism. Proc Natl Acad Sci U S A 2003, 100:2748-2753.
• [34]Badellino KO, Wolfe ML, Reilly MP, Rader DJ: Endothelial lipase concentrations are increased in metabolic syndrome and associated with coronary atherosclerosis. PLoS Med 2006, 3:e22.
• [35]Fang YQ, Huang L, Li AM, Song YM, Jin J, Geng ZH, Yu XJ, Deng MY: Significance of the ratio of circulating endothelial cell expressing endothelial lipase and supersensitivity C-reactive protein in prognosis of patients with coronary artery disease. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue 2007, 19:644-646.
• [36]McCy MG, Sun GS, Marchadier D, Maugeais C, Glick JM, Rader DJ: Characterization of the lipolytic activity of endothelial lipase. J Lipid Res 2002, 43:921-929.
• [37]Zhang B, Menzin J, Friedman M, Korn JR, Burge RT: Predicted coronary risk for adults with coronary heart disease and low HDL-C: an analysis from the US National Health and Nutrition Examination Survey. Curr Med Res Opin 2008, 24:2711-2717.
• [38]Badellino KO, Wolfe ML, Reilly MP, Rader DJ: Endothelial lipase is increased in vivo by inflammation in humans. Circulation 2008, 117:678-685.