Volume 10, Issue 4 (Vol.10 No.4 Jan 2022)                   rbmb.net 2022, 10(4): 580-588 | Back to browse issues page


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Karimi Z, Daneshmoghadam J, Ghaedi H, Khalili E, Panahi G, Shanaki* M. Association of rs2954029 and rs6982502 Variants with Coronary Artery Disease by HRM Technique: A GWAS Replication Study in an Iranian Population. rbmb.net. 2022; 10 (4) :580-588
URL: http://rbmb.net/article-1-666-en.html
Department of Clinical Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Abstract:   (1250 Views)
Background: Genome-wide association studies (GWAS) have been the primary tool for an unbiased study of the genetic background of coronary artery disease (CAD). They have identified a list of single-nucleotide polymorphisms (SNPs) associated with coronary artery disease (CAD). In this study, we aimed to replicate the association of rs2954029 and rs6982502, a GWAS identified SNP, to CAD in an Iranian population.

Methods: A sample of 285 subjects undergoing coronary angiography, including 134 CAD patients and 151 healthy. The genotype determination of rs2954029 and rs6982502 SNPs performed using the high-resolution melting analysis (HRM) technique. 

Results: Our results revealed that the TT genotype of rs2954029 (p= 0.009) and rs6982502 (p< 0.001) were significantly higher in CAD patients compared with controls. Binary logistic regression showed that rs6982502 and rs2954029 increase the risk of CAD incidence (2.470 times, p= 0.011, 95% CI= [1.219-4.751], and 2.174 times, p= 0.033, 95% CI= [1.066-4.433] respectively). After adjusting for confounders, we found that rs6982502 and rs2954029 are significantly associated with CAD risk.

Conclusions: These data showed that the TT genotype of rs2954029 and rs6982502 is associated with the risk of CAD in a hospital-based sample of the Iranian population, which has replicated the result of recent GWAS studies.
Full-Text [PDF 260 kb]   (542 Downloads)    
Type of Article: Case Report | Subject: Cell Biology
Received: 2021/03/1 | Accepted: 2021/05/8 | Published: 2022/02/7

References
1. Rashid MA, Edwards D, Walter FM, Mant J. Medication taking in coronary artery disease: a systematic review and qualitative synthesis. Ann Fam Med. 2014;12(3):224-32. [DOI:10.1370/afm.1620] [PMID] [PMCID]
2. Shanaki M, Hossein-Nezhad A, Meshkani R, Beigy M, Shirzad M, Pasalar P, et al. Effects of resveratrol on crosstalk between canonical Β-catenin/Wnt and FOXO pathways in coronary artery disease patients with metabolic syndrome: a case control study. Iran J Pharm Res. 2016;15(3):547-559.
3. Rafieian-Kopaei M, Setorki M, Doudi M, Baradaran A, Nasri H. Atherosclerosis: process, indicators, risk factors and new hopes. Int J Prev Med. 2014;5(8):927-46.
4. Ebrahimi M, Kazemi-Bajestani S, Ghayour-Mobarhan M, Ferns G. Coronary artery disease and its risk factors status in Iran: a review. Iran Red Crescent Med J. 2011;13(9):610-23. [DOI:10.5812/kowsar.20741804.2286] [PMID] [PMCID]
5. Kazemi T, Sharifzadeh G, Javadinia SA, Salehiniya H. Prevalence of cardiovascular risk factors among the nurse population in the east of Iran. International Journal of Travel Medicine and Global Health. 2015;3(4):133-136. [DOI:10.20286/ijtmgh-030477]
6. Yang X, Li Y, Li Y, Ren X, Zhang X, Hu D, et al. Oxidative stress-mediated atherosclerosis: mechanisms and therapies. Front Physiol. 2017;8:600. [DOI:10.3389/fphys.2017.00600] [PMID] [PMCID]
7. Bampali K, Mouzarou A, Lamnisou K, Babalis D. Genetics and coronary artery disease: present and future. Hellenic J Cardiol. 2014;55(2):156-63.
8. Cen J, Xiong Q, Yang X, Guo J, Xiong X-d, Zhang A. Pri-miR-34b/c rs4938723 Polymorphism Contributes to Coronary Artery Disease Susceptibility. Arch Med Res. 2019;50(4):170-174. [DOI:10.1016/j.arcmed.2019.07.009] [PMID]
9. Peden JF, Farrall M. Thirty-five common variants for coronary artery disease: the fruits of much collaborative labour. Hum Mol Genet. 2011;20(R2):R198-205. [DOI:10.1093/hmg/ddr384] [PMID] [PMCID]
10. Deloukas P, Kanoni S, Willenborg C, Farrall M, Assimes TL, Thompson JR, et al. Large-scale association analysis identifies new risk loci for coronary artery disease. Nat Genet. 2011;43(4):333-338. [DOI:10.1038/ng.784] [PMID] [PMCID]
11. Jadhav KS, Bauer RC. Trouble With Tribbles-1: Elucidating the Mechanism of a Genome-Wide Association Study Locus. Arteriosclerosis, thrombosis, and vascular biology. 2019;39(6):998-1005. [DOI:10.1161/ATVBAHA.118.311573] [PMID] [PMCID]
12. Kessler T, Vilne B, Schunkert H. The impact of genome‐wide association studies on the pathophysiology and therapy of cardiovascular disease. EMBO Mol Med. 2016;8(7):688-701. [DOI:10.15252/emmm.201506174] [PMID] [PMCID]
13. Nikpay M, Goel A, Won H-H, Hall LM, Willenborg C, Kanoni S, et al. A comprehensive 1000 Genomes-based genome-wide association meta-analysis of coronary artery disease. Nat Genet. 2015;47(10):1121-1130. [DOI:10.1038/ng.3396] [PMID] [PMCID]
14. van der Harst P, Verweij N. Identification of 64 novel genetic loci provides an expanded view on the genetic architecture of coronary artery disease. Circ Res. 2018;122(3):433-443. [DOI:10.1161/CIRCRESAHA.117.312086] [PMID] [PMCID]
15. Douvris A, Soubeyrand S, Naing T, Martinuk A, Nikpay M, Williams A, et al. Functional Analysis of the TRIB 1 Associated Locus Linked to Plasma Triglycerides and Coronary Artery Disease. J Am Heart Assoc. 2014;3(3):e000884. [DOI:10.1161/JAHA.114.000884] [PMID] [PMCID]
16. Nelson CP, Goel A, Butterworth AS, Kanoni S, Webb TR, Marouli E, et al. Association analyses based on false discovery rate implicate new loci for coronary artery disease. Nat Genet. 2017;49(9):1385-1391. [DOI:10.1038/ng.3913] [PMID]
17. Bauer RC, Yenilmez BO, Rader DJ. Tribbles-1: a novel regulator of hepatic lipid metabolism in humans. Biochem Soc Trans. 2015;43(5):1079-84. [DOI:10.1042/BST20150101] [PMID] [PMCID]
18. Nasiri H, Forouzandeh M, Rasaee M, Rahbarizadeh F. Modified salting‐out method: high‐yield, high‐quality genomic DNA extraction from whole blood using laundry detergent. J Clin Lab Anal. 2005;19(6):229-32. [DOI:10.1002/jcla.20083] [PMID] [PMCID]
19. Rivero ER, Neves AC, Silva-Valenzuela MG, Sousa SO, Nunes FD. Simple salting-out method for DNA extraction from formalin-fixed, paraffin-embedded tissues. Pathol Res Pract. 2006;202(7):523-9. [DOI:10.1016/j.prp.2006.02.007] [PMID]
20. Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CJ. Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data. Lancet. 2006;367(9524):1747-57. [DOI:10.1016/S0140-6736(06)68770-9]
21. Samani NJ, Erdmann J, Hall AS, Hengstenberg C, Mangino M, Mayer B, et al. Genomewide association analysis of coronary artery disease. N Engl J Med. 2007;357(5):443-53. [DOI:10.1056/NEJMoa072366] [PMID] [PMCID]
22. Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, et al. Investigators IS. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004;364(9438):937-52. [DOI:10.1016/S0140-6736(04)17018-9]
23. Munz M, Richter GM, Loos BG, Jepsen S, Divaris K, Offenbacher S, et al. Genome-wide association meta-analysis of coronary artery disease and periodontitis reveals a novel shared risk locus. Sci Rep. 2018;8(1):13678. [DOI:10.1038/s41598-018-31980-8] [PMID] [PMCID]
24. Jones PD, Webb TR. From GWAS to new biology and treatments in CAD. Aging (Albany NY). 2019;11(6):1611-1612. [DOI:10.18632/aging.101891] [PMID] [PMCID]
25. Ram R, Wakil S, Muiya N, Andres E, Mazhar N, Hagos S, et al. A common variant association study in ethnic Saudi Arabs reveals novel susceptibility loci for hypertriglyceridemia. Clin Genet. 2017;91(3):371-378. [DOI:10.1111/cge.12859] [PMID]
26. Ishizuka Y, Nakayama K, Ogawa A, Makishima S, Boonvisut S, Hirao A, et al. TRIB1 downregulates hepatic lipogenesis and glycogenesis via multiple molecular interactions. J Mol Endocrinol. 2014;52(2):145-58. [DOI:10.1530/JME-13-0243] [PMID]
27. Varbo A, Benn M, Tybjærg-Hansen A, Grande P, Nordestgaard BG. TRIB1 and GCKR polymorphisms, lipid levels, and risk of ischemic heart disease in the general population. Arterioscler Thromb Vasc Biol. 2011;31(2):451-7. [DOI:10.1161/ATVBAHA.110.216333] [PMID]
28. Zhang Z, Tao L, Chen Z, Zhou D, Kan M, Zhang D, et al. Association of genetic loci with blood lipids in the Chinese population. PLoS One. 2011;6(11):e27305. [DOI:10.1371/journal.pone.0027305] [PMID] [PMCID]
29. Ikeoka T, Hayashida N, Nakazato M, Sekita T, Murata-Mori F, Ando T, et al. The A> T polymorphism of the tribbles homolog 1 gene is associated with serum triglyceride concentrations in Japanese community-dwelling women. Tohoku J Exp Med. 2014;233(2):149-53. [DOI:10.1620/tjem.233.149] [PMID]
30. Cheema AN, Rosenthal SL, Kamboh IM. Proficiency of data interpretation: identification of signaling SNPs/specific loci for coronary artery disease. Database. 2017;2017. [DOI:10.1093/database/bax078] [PMID] [PMCID]
31. Willer CJ, Sanna S, Jackson AU, Scuteri A, Bonnycastle LL, Clarke R, et al. Newly identified loci that influence lipid concentrations and risk of coronary artery disease. Nat Genet. 2008;40(2):161-9. [DOI:10.1038/ng.76] [PMID] [PMCID]
32. Teslovich TM, Musunuru K, Smith AV, Edmondson AC, Stylianou IM, Koseki M, et al. Biological, clinical and population relevance of 95 loci for blood lipids. Nature. 2010;466(7307):707-713. [DOI:10.1038/nature09270] [PMID] [PMCID]
33. Waterworth DM, Ricketts SL, Song K, Chen L, Zhao JH, Ripatti S, et al. Genetic variants influencing circulating lipid levels and risk of coronary artery disease. Arterioscler Thromb Vasc Biol. 2010;30(11):2264-76. [DOI:10.1161/ATVBAHA.109.201020] [PMID] [PMCID]
34. Hegedus Z, Czibula A, Kiss-Toth E. Tribbles: a family of kinase-like proteins with potent signalling regulatory function. Cell Signal. 2007;19(2):238-50. [DOI:10.1016/j.cellsig.2006.06.010] [PMID]
35. Vilkeviciute A, Kriauciuniene L, Chaleckis R, Deltuva VP, Liutkeviciene R. RAD51B (rs8017304 and rs2588809), TRIB1 (rs6987702, rs4351379, and rs4351376), COL8A1 (rs13095226), and COL10A1 (rs1064583) gene variants with predisposition to age-related macular degeneration. Dis Markers. 2019;2019:5631083. [DOI:10.1155/2019/5631083] [PMID] [PMCID]
36. Iwamoto S, Boonvisut S, Makishima S, Ishizuka Y, Watanabe K, Nakayama K. The role of TRIB1 in lipid metabolism; from genetics to pathways. Biochem Soc Trans. 2015;43(5):1063-8. 37. Consortium IKC. Large-scale gene-centric analysis identifies novel variants for coronary artery disease. PLoS Genet. 2011;7(9):e1002260. [DOI:10.1042/BST20150094] [PMID]
37. Sung HY, Guan H, Czibula A, King AR, Eder K, Heath E, et al. Human tribbles-1 controls proliferation and chemotaxis of smooth muscle cells via MAPK signaling pathways. J Biol Chem. 2007;282(25):18379-18387. [DOI:10.1074/jbc.M610792200] [PMID] [PMCID]
38. Sallam T, Sandhu J, Tontonoz P. Long noncoding RNA discovery in cardiovascular disease: decoding form to function. Circ Res. 2018;122(1):155-166. [DOI:10.1161/CIRCRESAHA.117.311802] [PMID] [PMCID]

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