Effects of MPO‑463G/A and ‑129G/A polymorphisms on coronary artery disease risk and patient survival in a Turkish population

Arslan,Serdal; Berkan,Öcal; Bayyurt,Burcu; Beton,Osman; Şahin,Ni̇l  Özbi̇lüm; Aydemir,Eylem  Itır

doi:10.3892/br.2017.995

Effects of MPO‑463G/A and ‑129G/A polymorphisms on coronary artery disease risk and patient survival in a Turkish population

Authors:
- Serdal Arslan
- Öcal Berkan
- Burcu Bayyurt
- Osman Beton
- Ni̇l Özbi̇lüm Şahin
- Eylem Itır Aydemir
View Affiliations

Affiliations: Department of Medical Biology, Faculty of Medicine, Cumhuriyet University, 58140 Sivas, Turkey, Department of Cardiovascular Surgery, Heart Center, Cumhuriyet University, 58140 Sivas, Turkey, Department of Cardiology, Heart Center, Cumhuriyet University, 58140 Sivas, Turkey, Department of Molecular Biology and Genetics, Faculty of Science, Cumhuriyet University, 58140 Sivas, Turkey, Department of Statistics, Faculty of Science, Cumhuriyet University, 58140 Sivas, Turkey
Published online on: October 3, 2017 https://doi.org/10.3892/br.2017.995
Pages: 547-552

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

Myeloperoxidase (MPO) is an oxidative hemoprotein compound expressed in polymorphonuclear leukocytes that contributes to inflammatory responses. Coronary artery disease (CAD), as the most prevalent form of heart disease, is considered to originate from an interaction between genetic and environmental factors. In the present study, the potential associations between MPO‑463G/A and ‑129G/A polymorphisms with CAD were investigated in a Turkish population using a polymerase chain reaction‑based restriction fragment length polymorphism (RFLP) assay technique. To the best of our knowledge, the study was the first to examine the association of MPO‑463G/A and ‑129G/A with patient survival rate in a Turkish population. The study population consisted of 201 patients with CAD and 201 healthy controls. The results indicated that there was a significant association of the GA genotype of MPO‑463G/A with the case population (P=0.048). Meanwhile, in the patients with CAD, the frequency distributions of the MPO‑129A allele (P=0.006) and GA genotype (P=0.001) were significantly increased compared with the G allele and GG genotype, respectively, in CAD patients. Additionally, compared with the GG genotype, the frequency distribution of MPO‑129A was significantly increased in the patient group regarding smoking status (P=0.001) and the presence of hypercholesterolemia (P=0.028). However, survival analysis did not detect an effect of either polymorphism on the survival rate of the CAD patients (P>0.05). Therefore, the MPO‑129GA genotype may be a significant risk factor for the development of CAD.

View Figures

View References

1	Grimes DS: An epidemic of coronary heart disease. QJM. 105:509–518. 2012. View Article : Google Scholar : PubMed/NCBI
2	Hansson GK: Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 352:1685–1695. 2005. View Article : Google Scholar : PubMed/NCBI
3	Naghavi M, Libby P, Falk E, Casscells SW, Litovsky S, Rumberger J, Badimon JJ, Stefanadis C, Moreno P, Pasterkamp G, et al: From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. Circulation. 108:1664–1672. 2003. View Article : Google Scholar : PubMed/NCBI
4	Roman RM, Wendland AE and Polanczyk CA: Myeloperoxidase and coronary arterial disease: From research to clinical practice. Arq Bras Cardiol. 91:e11–e19. 2008.PubMed/NCBI
5	Morishita K, Tsuchiya M, Asano S, Kaziro Y and Nagata S: Chromosomal gene structure of human myeloperoxidase and regulation of its expression by granulocyte colony-stimulating factor. J Biol Chem. 262:15208–15213. 1987.PubMed/NCBI
6	Piedrafita FJ, Molander RB, Vansant G, Orlova EA, Pfahl M and Reynolds WF: An Alu element in the myeloperoxidase promoter contains a composite SP1-thyroid hormone-retinoic acid response element. J Biol Chem. 271:14412–14420. 1996. View Article : Google Scholar : PubMed/NCBI
7	Pecoits-Filho R, Stenvinkel P, Marchlewska A, Heimburger O, Bárány P, Hoff CM, Holmes CJ, Suliman M, Lindholm B, Schalling M and Nordfors L: A functional variant of the myeloperoxidase gene is associated with cardiovascular disease in end-stage renal disease patients. Kidney Int Suppl. 84:S172–S176. 2003. View Article : Google Scholar
8	Davies MJ, Hawkins CL, Pattison DI and Rees MD: Mammalian heme peroxidases: From molecular mechanisms to health implications. Antioxid Redox Signal. 10:1199–1234. 2008. View Article : Google Scholar : PubMed/NCBI
9	Hampton MB, Kettle AJ and Winterbourn CC: Inside the neutrophil phagosome: Oxidants, myeloperoxidase, and bacterial killing. Blood. 92:3007–3017. 1998.PubMed/NCBI
10	Verdecchia P, Angeli F, Cavallini C, Mazzotta G, Garofoli M, Martire P and Reboldi G: The optimal blood pressure target for patients with coronary artery disease. Curr Cardiol Rep. 12:302–306. 2010. View Article : Google Scholar : PubMed/NCBI
11	Cannon CP and Vierck E: The New Heart Disease Handbook. 1st edition. Fair Winds Press; Beverly, MA: 2009
12	Sambrook J, Fritsch EF and Maniatis T: Molecular Cloning - A Laboratory Manual. 2nd edition. Cold Spring Harbor Laboratory Press; Cold Spring Harbor, NY: 1989
13	Arslan S, Pinarbasi H and Silig Y: Myeloperoxidase G-463A polymorphism and risk of lung and prostate cancer in a Turkish population. Mol Med Rep. 4:87–92. 2011.PubMed/NCBI
14	Lozano R, Naghavi M, Foreman K, Lim S, Shibuya K, Aboyans V, Abraham J, Adair T, Aggarwal R, Ahn SY, et al: Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet. 380:2095–2128. 2012. View Article : Google Scholar : PubMed/NCBI
15	Lusis AJ, Mar R and Pajukanta P: Genetics of atherosclerosis. Annu Rev Genomics Hum Genet. 5:189–218. 2004. View Article : Google Scholar : PubMed/NCBI
16	Steinberg D and Witztum JL: Is the oxidative modification hypothesis relevant to human atherosclerosis? Do the antioxidant trials conducted to date refute the hypothesis? Circulation. 105:2107–2111. 2002. View Article : Google Scholar : PubMed/NCBI
17	Hillegass LM, Griswold DE, Brickson B and Albrightson-Winslow C: Assessment of myeloperoxidase activity in whole rat kidney. J Pharmacol Methods. 24:285–295. 1990. View Article : Google Scholar : PubMed/NCBI
18	Nikpoor B, Turecki G, Fournier C, Théroux P and Rouleau GA: A functional myeloperoxidase polymorphic variant is associated with coronary artery disease in French-Canadians. Am Heart J. 142:336–339. 2001. View Article : Google Scholar : PubMed/NCBI
19	Zotova E, Lyrenäs L, de Faire U, Morgenstern R, Gigante B and Bennet AM: The myeloperoxidase gene and its influence on myocardial infarction in a Swedish population: Protective role of the −129A allele in women. Coron Artery Dis. 20:322–326. 2009. View Article : Google Scholar : PubMed/NCBI
20	Ergen A, İsbir S, Timirci Ö, Tekeli A and İsbir T: Effects of myeloperoxidase −463 G/A gene polymorphism and plasma levels on coronary artery disease. Mol Biol Rep. 38:887–891. 2011. View Article : Google Scholar : PubMed/NCBI
21	Tang N, Wang Y and Mei Q: Myeloperoxidase G-463A polymorphism and susceptibility to coronary artery disease: A meta-analysis. Gene. 523:152–157. 2013. View Article : Google Scholar : PubMed/NCBI
22	Borges FK, Borges FK, Stella SF, Souza JF, Wendland AE, Werres Junior LC, Ribeiro JP and Polanczyk CA: Serial analyses of C-reactive protein and myeloperoxidase in acute coronary syndrome. Clin Cardiol. 32:E58–E62. 2009. View Article : Google Scholar : PubMed/NCBI
23	Nicholls SJ and Hazen SL: Myeloperoxidase and cardiovascular disease. Arterioscler Thromb Vasc Biol. 25:1102–1111. 2005. View Article : Google Scholar : PubMed/NCBI
24	Puddu P, Cravero E, Puddu GM and Muscari A: Genes and atherosclerosis: At the origin of the predisposition. Int J Clin Pract. 59:462–472. 2005. View Article : Google Scholar : PubMed/NCBI
25	Mocatta TJ, Pilbrow AP, Cameron VA, Senthilmohan R, Frampton CM, Richards AM and Winterbourn CC: Plasma concentrations of myeloperoxidase predict mortality after myocardial infarction. J Am Coll Cardiol. 49:1993–2000. 2007. View Article : Google Scholar : PubMed/NCBI
26	Meuwese MC, Stroes ES, Hazen SL, van Miert JN, Kuivenhoven JA, Schaub RG, Wareham NJ, Luben R, Kastelein JJ, Khaw KT and Boekholdt SM: Serum myeloperoxidase levels are associated with the future risk of coronary artery disease in apparently healthy individuals: The EPIC-Norfolk Prospective Population Study. J Am Coll Cardiol. 50:159–165. 2007. View Article : Google Scholar : PubMed/NCBI
27	Finegold JA, Asaria P and Francis DP: Mortality from ischaemic heart disease by country, region, and age: Statistics from World Health Organisation and United Nations. Int J Cardiol. 168:934–945. 2013. View Article : Google Scholar : PubMed/NCBI
28	Maddhuri S, Pallapolu P, Bandaru S, Suresh G, Malempati AR, Jyothy A and Mundluru HP: Analysis of plasma myeloperoxidase levels and functional gene −463G>A and −129G>A polymorphisms with early onset of coronary artery disease in South Indian population. Folia Cardiol. 11:272–278. 2016. View Article : Google Scholar
29	Li YY, Wang H, Qian J, Kim HJ, Wu JJ, Wang LS, Zhou CW, Yang ZJ and Lu XZ: PRISMA-combined Myeloperoxidase −463G/A gene polymorphism and coronary artery disease: A meta-analysis of 4744 subjects. Medicine (Baltimore). 96:e64612017. View Article : Google Scholar : PubMed/NCBI