The association between CYP1A1 genetic polymorphisms and coronary artery disease in the Uygur and Han of China

Lipids in Health and Disease

Bang-Dang Chen¹  Fen Liu¹  Dilare Adi¹  Shuo Pan¹  Yi-Ning Yang²  Xiang Xie¹  Yi-Tong Ma²  Jin-Guo Zou¹ 

[1] Xinjiang Key Laboratory of Cardiovascular Disease Research, Urumqi 830054, People’s Republic of China;Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, People’s Republic of China

关键词: Case–control study;    Coronary artery disease;    Single nucleotide polymorphism;    CYP1A1;   

Others  :  1152051
DOI  :  10.1186/1476-511X-13-145

 received in 2014-07-10, accepted in 2014-09-02,  发布年份 2014

【 摘 要 】

Background

The cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1) gene is expressed in the vascular endothelium, which metabolizes arachidonic acid into 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs). 20-HETE mediates cardiovascular homeostasis and growth response in vascular smooth muscle cells (VSMCs) as well as the anti-platelet effect. EETs are potent endogenous vasodilators and inhibitors of vascular inflammation. This study assessed the association between human CYP1A1 gene polymorphisms and coronary artery disease (CAD) in the Uygur and Han in China.

Methods

Two independent case–control studies that recruited Han (389 patients with CAD and 411 controls) and Uygur participants (293 patients with CAD and 408 controls) analyzed the relationship between CYP1A1 single nucleotide polymorphisms (SNPs: rs4886605, rs12441817, rs4646422 and rs1048943) and CAD. All patients with CAD and controls were genotyped for the four SNPs of CYP1A1 using TaqMan SNP genotyping assays.

Results

In the Uygur group, the distribution of the dominant model(CC vs CT + TT) of rs4886605 for the total sample and the males was significantly different between CAD patients and control participants (P = 0.001 and P = 0.012, respectively), The difference remained significant after a multivariate adjustment (P = 0.018, P = 0.015, respectively). The rs12441817 was also associated with CAD in a dominant model for all participants (P = 0.003) and men (P = 0.012), and the difference remained significant after a multivariate adjustment (P = 0.016, P = 0.002, respectively). However, we did not observe differences in the Uygur females and Han group with regard to the allele frequency or genotypic distribution of rs4886605 and rs12441817 between patients with CAD and control participants. Patients with CAD did not significantly differ from the control participants with regard to the distributions of rs4646422 and rs1048943 genotypes, the dominant model, the recessive model, or allele frequency in the Han and Uygur groups.

Conclusion

Both rs4886605 and rs12441817 SNPs of the CYP1A1 gene are associated with CAD in the Uygur population of China.

【 授权许可】

   
2014 Zou et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

【 参考文献 】

• [1]Zordoky BNM, El-Kadi AOS: Effect of cytochrome P450 polymorphism on arachidonic acid metabolism and their impact on cardiovascular diseases. Pharmacol Ther 2010, 125:446-463.
• [2]Aboutabl ME, El-Kadi AOS: Constitutive expression and inducibility of CYP1A1 in the h9c2 rat cardiomyoblast cells. Toxicol In Vitro 2007, 21(8):1686-1691.
• [3]Frazier L, Johnson RL, Sparks E: Genomics and cardiovascular disease. J Nurs Scholarsh 2005, 37(4):315-321.
• [4]Nordlie MA, Wold LE, Kloner RA: Genetic contributors toward increased risk for ischemic heart disease. J Mol Cell Cardiol 2005, 39(4):667-679.
• [5]Winkelmann BR, Hager J: Genetic variation in coronary heart disease and myocardial infarction: methodological overview and clinical evidence. Pharmacogenomics 2000, 1(1):73-94.
• [6]Niwa T, Murayama N, Yamazaki H: Oxidation of endobiotics mediated by xenobiotic-metabolizing forms of human cytochrome P450. Curr Drug Metab 2009, 10(7):700-712.
• [7]Elbekai RH, El-Kadi AO: Cytochrome P450 enzymes: central players in cardiovascular health and disease. Pharmacol Ther 2006, 112(2):564-587.
• [8]Zordoky BN, El-Kadi AO: Modulation of cardiac and hepatic cytochrome P450 enzymes during heart failure. Curr Drug Metab 2008, 9(2):122-128.
• [9]Wang XL, Greco M, Sim AS, Duarte N, Wang J, Wilcken DE: Effect of CYP1A1 MspI polymorphism on cigarette smoking related coronary artery disease and diabetes. Atherosclerosis 2002, 162(2):391-397.
• [10]Cornelis MC, El-Sohemy A, Campos H: Genetic polymorphism of CYP1A2 increases the risk of myocardial infarction. J Med Genet 2004, 41(10):758-762.
• [11]Yasar U, Bennet AM, Eliasson E, Lundqren S, Wiman B, De Faire U, Rane A: Allelic variants of cytochromes P450 2C modify the risk for acute myocardial infarction. Pharmacogenetics 2003, 13(12):715-720.
• [12]Funk M, Endler G, Freitag R, Wojta J, Huber K, Mannhalter C, Sunder-Plassmann R: CYP2C9*2 and CYP2C9*3 alleles confer a lower risk for myocardial infarction. Clin Chem 2004, 50(12):2395-2398.
• [13]Spiecker M, Darius H, Hankeln T, Soufi M, Sattler AM, Schaefer JR, Node K, Börgel J, Mügge A, Lindpaintner K, Huesing A, Maisch B, Zeldin DC, Liao JK: Risk of coronary artery disease associated with polymorphism of the cytochrome P450 epoxygenase CYP2J2. Circulation 2004, 110(15):2132-2136.
• [14]Nakayama T, Soma M, Saito S, Honye J, Yajima J, Rahmutula D, Kaneko Y, Sato M, Uwabo J, Aoi N, Kosuge K, Kunimoto M, Kanmatsuse K, Kokubun S: Association of a novel single nucleotide polymorphism of the prostacyclin synthase gene with myocardial infarction. Am Heart J 2002, 143(5):797-801.
• [15]Hengstenberg C, Holmer SR, Mayer B, Löwel H, Engel S, Hense HW, Riegger GA, Schunkert H: Evaluation of the aldosterone synthase (CYP11B2) gene polymorphism in patients with myocardial infarction. Hypertension 2000, 35(3):704-709.
• [16]Letonja M, Peterlin B, Bregar D, Petrovic D: Are the T/C polymorphism of the CYP17 gene and the tetranucleotide repeat (TTTA) polymorphism of the CYP19 gene genetic markers for premature coronary artery disease in Caucasians? Folia Biol (Praha) 2005, 51:76-81.
• [17]Choudhary D, Jansson I, Stoilov I, Sarfarazi M, Schenkman JB: Metabolism of retinoids and arachidonic acid by human and mouse cytochrome P450 1B1. Drug Metab Dispos 2004, 32(8):840-847.
• [18]Schwarz D, Kisselev P, Ericksen SS, Szklarz GD, Chernogolov A, Honeck H, Schunck WH, Roots I: Arachidonic and eicosapentaenoic acid metabolism by human CYP1A1: highly stereoselective formation of 17(r), 18(s)-epoxyeicosatetraenoic acid. Biochem Pharmacol 2004, 67(8):1445-1457.
• [19]Rifkind AB: CYP1A in TCDD toxicity and in physiology-with particular reference to CYP dependent arachidonic acid metabolism and other endogenous substrates. Drug Metab Rev 2006, 38(1–2):291-335.
• [20]Fleming I: Cytochrome P-450 under pressure: more evidence for a link between 20-hydroxyeicosatetraenoic acid and hypertension. Circulation 2005, 111(1):5-7.
• [21]Manfredi S, Federici C, Picano E, Botto N, Rizza A, Andreassi MG: GSTM1, GSTT1 and CYP1A1 detoxification gene polymorphisms and susceptibility to smoking-related coronary artery disease: a case-only study. Mutat Res 2007, 621(1–2):106-112.
• [22]Franchi E, Marino P, Biondi-Zoccai GG: Transradial versus transfemoral approach for percutaneous coronary procedures. Curr Cardiol Rep 2009, 11(5):391-397.
• [23]Vazquez B, Rios A, Escalante B: Arachidonic acid metabolism modulates vasopressin-induced renal vasoconstriction. Life Sci 1995, 56(18):1455-1466.
• [24]Chu ZM, Croft KD, Kingsbury DA, Falck JR, Reddy KM, Beilin LJ: Cytochrome P450 metabolites of arachidonic acid may be important mediators in angiotensin II-induced vasoconstriction in the rat mesentery in vivo. Clin Sci (Lond) 2000, 98(3):277-282.
• [25]Imig JD, Pham BT, LeBlanc EA, Reddy KM, Falck JR, Inscho EW: Cytochrome P450 and cyclooxygenase metabolites contribute to the endothelin-1 afferent arteriolar vasoconstrictor and calcium responses. Hypertension 2000, 35(1 pt 2):307-312.
• [26]Fu Z, Nakayama T, Sato N, Izumi Y, Kasamaki Y, Shindo A, Ohta M, Soma M, Aoi N, Sato M, Matsumoto K, Ozawa Y, Ma Y: Haplotype-based case study of human CYP4A11 gene and cerebral infarction in Japanese subject. Endocrine 2008, 33(2):215-222.
• [27]Uddin MR, Muthalif MM, Karzoun NA, Benter IF, Malik KU: Cytochrome P-450 metabolites mediate norepinephrine-induced mitogenic signaling. Hypertension 1998, 31(2):242-247.
• [28]Muthalif MM, Karzoun NA, Gaber L, Khandekar Z, Benter IF, Saeed AE, Parmentier JH, Estes A, Malik KU: Angiotensin II-induced hypertension: contribution of Ras GTPase/Mitogen-activated protein kinase and cytochrome P450 metabolites. Hypertension 2000, 36(4):604-609.
• [29]Schwartzman ML, Abraham NG, Masferrer J, Dunn MW, McGiff JC: Cytochrome P450 dependent metabolism of arachidonic acid in bovine corneal epithelium. Biochem Biophys Res Commun 1985, 132(1):343-351.
• [30]Quigley R, Baum M, Reddy KM, Griener JC, Falck JR: Effects of 20-HETE and 19(S)-HETE on rabbit proximal straight tubule volume transport. Am J Physiol Renal Physiol 2000, 278(6):949-953.
• [31]McGiff JC, Quilley J: 20-Hydroxyeicosatetraenoic acid and epoxyeicosatrie noic acids and blood pressure. Curr Opin Nephrol Hypertens 2001, 10(2):231-237.
• [32]Gross GJ, Falck JR, Gross ER, Isbell M, Moore J, Nithipatikom K: Cytochrome P450 and arachidonic acid metabolites: role in myocardial ischemia/reperfusion injury revisited. Cardiovasc Res 2005, 68(1):18-25.
• [33]Nithipatikom K, Gross ER, Endsley MP, Moore JM, Isbell MA, Falck JR, Campbell WB, Gross GJ: Inhibition of cytochrome P450omega-hydroxylase: a novel endogenous cardioprotective pathway. Circ Res 2004, 95(8):e65-e71.
• [34]Hill E, Fitzpatrick F, Murphy RC: Biological activity and metabolism of 20-hydroxyeicosatetraenoic acid in the human platelet. Br J Pharmacol 1992, 106(2):267-274.
• [35]Spiecker M, Liao JK: Cytochrome P450 epoxygenase CYP2J2 and the risk of coronary artery disease. Trends Cardiovasc Med 2006, 16:204-208. [PubMed]
• [36]Kawajiri K, Watanabe J, Hayashi S: Identification of allelic variants of the human CYP1A1 gene. Methods Enzymol 1996, 272:226-232.
• [37]Nerurkar PV, Okinaka L, Aoki C, Seifried A, Lum-Jones A, Wilkens LR, Le Marchand L: CYP1A1, GSTM1, and GSTP1 genetic polymorphisms and urinary 1-hydroxypyrene excretion in non-occupationally exposed individuals. Cancer Epidemiol Biomarkers Prev 2000, 9(10):1119-1122.
• [38]Yeh C-C, Sung F-C, Kuo L-T, Hsu WP, Chu HY: Polymorphisms of cytochrome P450 1A1, cigarette smoking and risk of coronary artery disease. Mutat Res 2009, 667:77-81.
• [39]Haschke-Becher E, Kirchheiner J, Trummer O, Grünbacher G, Kainz A: Impact of CYP2C8 and 2C9 polymorphisms on coronary artery disease and myocardial infarction in the LURIC cohort. Pharmacogenomics 2010, 11:1359-1365. [PubMed]
• [40]Kondo T, Hirose M, Kageyama K: Roles of oxidative stress and redox regulation in atherosclerosis. J Atheroscler Thromb 2009, 16:532-538. [PubMed]
• [41]Kaur-Knudsen D, Bojesen SE, Nordestgaard BG: Common polymorphisms in CYP2C9, sub-clinical atherosclerosis and risk of ischemic vascular disease in 52000 individuals. Pharmacogenomics J 2009, 9:327-332. [PubMed]
• [42]Tofovic SP: Estrogens and development of pulmonary hypertension Interaction of estradiol metabolism and pulmonary vascular disease. J Cardiovasc Pharmacol 2010, 56(6):696-708.