Association of the PSRC1 rs599839 Variant with Coronary Artery Disease in a Mexican Population
Abstract
:1. Introduction
2. Materials and Methods
2.1. Study Design
2.2. Clinical, Anthropometric, and Biochemical Evaluation
2.3. Marker Selection and Genotyping
2.4. Statistical Analysis
3. Results
4. Discussion
5. Conclusions
Author Contributions
Funding
Acknowledgments
Conflicts of Interest
References
- World Health Organization. World Health Statistics 2018: Monitoring Health for the SDGs, Sustainable Development Goals. Geneva. 2018. Available online: https://apps.who.int/iris/bitstream/handle/10665/272596/9789241565585-eng.pdf (accessed on 22 April 2020).
- Sanchis-Gomar, F.; Perez-Quilis, C.; Leischik, R.; Lucia, A. Epidemiology of coronary heart disease and acute coronary syndrome. Ann. Transl. Med. 2016, 4, 1–12. [Google Scholar] [CrossRef] [Green Version]
- Benjamin, E.J.; Virani, S.S.; Callaway, C.W.; Chamberlain, A.M.; Chang, A.R.; Cheng, S.; Chiuve, S.E.; Cushman, M.; Delling, F.N.; Deo, R.; et al. Heart disease and stroke statistics—2018 update: A report from the American Heart Association. Circulation 2018, 137, e67–e492. [Google Scholar] [CrossRef] [PubMed]
- Okrainec, K.; Banerjee, D.K.; Eisenberg, M.J. Coronary artery disease in the developing world. Am. Heart J. 2004, 148, 7–15. [Google Scholar] [CrossRef] [PubMed]
- Instituto Nacional de Estadística y Geografía (INEGI). Data of Méxicós general deaths from the INEGI. Available online: https://www.inegi.org.mx/sistemas/olap/Proyectos/bd/continuas/mortalidad/MortalidadGeneral.asp (accessed on 29 June 2020).
- Kumar, A.; Cannon, C.P. Acute coronary syndromes: Diagnosis and management, part I. Mayo Clin. Proc. 2009, 84, 917–938. [Google Scholar] [CrossRef] [Green Version]
- McPherson, R.; Tybjaerg-Hansen, A. Genetics of Coronary Artery Disease. Circ. Res. 2016, 118, 564–578. [Google Scholar] [CrossRef]
- Khera, A.V.; Kathiresan, S. Genetics of coronary artery disease: Discovery, biology and clinical translation. Nat. Rev. Genet. 2017, 18, 331–344. [Google Scholar] [CrossRef]
- 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, 433–443. [Google Scholar] [CrossRef]
- Dichgans, M.; Malik, R.; König, I.R.; Rosand, J.; Clarke, R.; Gretarsdottir, S.; Thorleifsson, G.; Mitchell, B.D.; Assimes, T.L.; Levi, C.; et al. Shared genetic susceptibility to ischemic stroke and coronary artery disease: A genome-wide analysis of common variants. Stroke 2014, 45, 24–36. [Google Scholar] [CrossRef] [Green Version]
- Schunkert, H.; König, I.R.; Kathiresan, S.; Reilly, M.P.; Assimes, T.L.; Holm, H.; Preuss, M.; Stewart, A.F.R.; Barbalic, M.; Gieger, C.; et al. Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease. Nat. Genet. 2011, 43, 333–338. [Google Scholar] [CrossRef]
- Erdmann, J.; Willenborg, C.; Nahrstaedt, J.; Preuss, M.; König, I.R.; Baumert, J.; Linsel-Nitschke, P.; Gieger, C.; Tennstedt, S.; Belcredi, P.; et al. Genome-wide association study identifies a new locus for coronary artery disease on chromosome 10p11.23. Eur. Heart J. 2011, 32, 158–168. [Google Scholar] [CrossRef] [Green Version]
- Samani, N.J.; Erdmann, J.; Hall, A.S.; Hengstenberg, C.; Mangino, M.; Mayer, B.; Dixon, R.J.; Meitinger, T.; Braund, P.; Wichmann, H.-E.; et al. Genomewide association analysis of coronary artery disease. N. Engl. J. Med. 2007, 357, 443–453. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Erdmann, J.; Großhennig, A.; Braund, P.S.; König, I.R.; Hall, A.S.; Linsel-nitschke, P.; Kathiresan, S.; Wright, B.; Tregouet, D.A.; Cambien, F.; et al. New susceptibility locus for coronary artery disease on chromosome 3q22.3. Nat. Genet. 2009, 41, 280–282. [Google Scholar] [CrossRef] [PubMed]
- Fujimaki, T.; Kato, K.; Oguri, M.; Yohida, T.; Horibe, H.; Yokoi, K.; Watanabe, S.; Satoh, K.; Aoyagi, Y.; Tanaka, M.; et al. Association of a polymorphism of BTN2A1 with dyslipidemia in East Asian populations. Exp. Ther. Med. 2011, 2, 745–749. [Google Scholar] [CrossRef] [PubMed]
- Yamada, Y.; Nishida, T.; Ichihara, S.; Sawabe, M.; Fuku, N.; Nishigaki, Y.; Aoyagi, Y.; Tanaka, M.; Fujiwara, Y.; Yoshida, H.; et al. Association of a polymorphism of BTN2A1 with myocardial infarction in East Asian populations. Atherosclerosis 2011, 215, 145–152. [Google Scholar] [CrossRef] [PubMed]
- Yusuf, S.; Hawken, S.; Ounpuu, S.; Dans, T.; Avezum, A.; Lanas, F.; McQueen, M.; Budaj, A.; Pais, P.; Varigos, J.; et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. Lancet 2004, 364, 937–952. [Google Scholar] [CrossRef]
- Preuss, M.; König, I.R.; Thompson, J.R.; Erdmann, J.; Absher, D.; Assimes, T.L.; Blankenberg, S.; Boerwinkle, E.; Chen, L.; Cupples, A.L.; et al. Design of the Coronary ARtery DIsease Genome-Wide Replication And Meta-Analysis (CARDIoGRAM) Study: A Genome-wide association meta-analysis involving more than 22,000 cases and 60,000 controls. Circ. Cardiovasc. Genet. 2010, 3, 475–483. [Google Scholar] [CrossRef]
- Sirtori, C.R. The pharmacology of statins. Pharmacol Res. 2014, 88, 3–11. [Google Scholar] [CrossRef]
- Oesterle, A.; Laufs, U.; Liao, J.K. Pleiotropic Effects of Statins on the Cardiovascular System. Circ Res. 2017, 120, 229–243. [Google Scholar] [CrossRef] [Green Version]
- Guo, J.; Luo, Y.X.; Tao, L.X.; Guo, X.H. Association between 1p13.3 genomic markers and coronary artery disease: A meta-analysis involving patients and controls. Genet. Mol Res. 2015, 14, 9092–9102. [Google Scholar] [CrossRef]
- Arvind, P.; Nair, J.; Jambunathan, S.; Kakkar, V.V.; Shanker, J. CELSR2-PSRC1-SORT1 gene expression and association with coronary artery disease and plasma lipid levels in an Asian Indian cohort. J. Cardiol. 2014, 64, 339–346. [Google Scholar] [CrossRef] [Green Version]
- Rizk, N.M.; El-Menyar, A.; Egue, H.; Wais, I.S.; Baluli, H.M.; Alali, K.; Farag, F.; Younes, N.; Al Suwaidi, J. The association between serum LDL cholesterol and genetic variation in chromosomal locus 1p13.3 among coronary artery disease patients. Biomed. Res. Int. 2015, 2015, 1–12. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Abe, S.; Tokoro, F.; Matsuoka, R.; Arai, M.; Noda, T.; Watanabe, S.; Horibe, H.; Fujimaki, T.; Oguri, M.; Kato, K.; et al. Association of genetic variants with dyslipidemia. Mol. Med. Rep. 2015, 12, 5429–5436. [Google Scholar] [CrossRef] [PubMed]
- Carlo, A.S.; Nykjaer, A.; Willnow, T.E. Sorting receptor sortilin—A culprit in cardiovascular and neurological diseases. J. Mol. Med. 2014, 92, 905–911. [Google Scholar] [CrossRef] [PubMed]
- Musunuru, K.; Strong, A.; Frank-kamenetsky, M.; Lee, N.E.; Ahfeldt, T.; Sachs, K.V.; Li, X.; Li, H.; Kuperwasser, N.; Ruda, V.; et al. From noncoding variant to phenotype via SORT1 at the 1p13 cholesterol locus. Nature 2010, 466, 714–719. [Google Scholar] [CrossRef] [PubMed]
- Han, W.; Wei, Z.; Zhang, H.; Geng, C.; Dang, R.; Yang, M.; Zhang, J.; Wang, C.; Jiang, P. The association between sortilin and inflammation in patients with coronary heart disease. J. Inflamm. Res. 2020, 13, 71–79. [Google Scholar] [CrossRef] [Green Version]
- Linsel-Nitschke, P.; Heeren, J.; Aherrahrou, Z.; Bruse, P.; Gieger, C.; Illig, T.; Prokisch, H.; Heim, K.; Doering, A.; Peters, A.; et al. Genetic variation at chromosome 1p13.3 affects sortilin mRNA expression, cellular LDL-uptake and serum LDL levels which translates to the risk of coronary artery disease. Atherosclerosis 2010, 208, 183–189. [Google Scholar] [CrossRef]
- Pfaff, C.L.; Parra, E.J.; Bonilla, C.; Hiester, K.; McKeigue, P.M.; Kamboh, M.I.; Hutchinson, R.G.; Ferrell, R.E.; Boerwinkle, E.; Shriver, M.D. Population structure in admixed populations: Effect of admixture dynamics on the pattern of linkage disequilibrium. Am. J. Hum. Genet. 2001, 68, 198–207. [Google Scholar] [CrossRef] [Green Version]
- Lu, Y.; Loos, R.J. Obesity genomics: Assessing the transferability of susceptibility loci across diverse populations. Genome Med. 2013, 5, 55. [Google Scholar] [CrossRef] [Green Version]
SNP | Gene | Chr:Position a | Phenotype b | Population c | Reference |
---|---|---|---|---|---|
rs599839 | PSRC1 | 1:109279544 | CAD, IS | EUR | [10,11,13] |
rs9818870 | MRAS | 3:138403280 | CAD | EUR | [10,14] |
rs6929846 | BTN2A1 | 6:26458037 | MI, Dyslipidemia | JAP | [15,16] |
rs6922269 | MTHFD1L | 6:150931849 | CAD | EUR | [13] |
rs1333049 | CDKN2B | 9:22125504 | CAD | EUR | [10,13,18] |
rs3739998 | KIAA1462 | 10:30027143 | CAD, MI | EUR | [12] |
rs501120 | CXCL12 | 10:44258419 | CAD | EUR | [13] |
rs2259816 | HNF1A | 12:120997784 | CAD | EUR | [14] |
Characteristic | Controls (n = 513) | CAD (n = 394) | p-Value |
---|---|---|---|
Age (years) | 59.7 (±9.6) | 59.8 (±7.7) | 0.866 |
BMI (kg/m2) | 28 (±4.7) | 27 (±3.8) | <0.001 |
Gender n (%) | <0.001 | ||
Male | 260 (50.7%) | 297 (75.3%) | |
Female | 253 (49.3%) | 97 (24.6%) | |
Glucose (mg/dL) | 114.0 (±51.1) | 151.2 (±90.1) | <0.001 |
HbA1c (%) | 6.16 (± 1.46) | 6.0 (±1.99) | 0.270 |
Total cholesterol (mg/dL) | 199.4 (± 51.2) | 188.8 (±75.5) | 0.014 |
Triglycerides (mg/dL) | 171.8 (± 113.1) | 174.4 (±91.8) | 0.718 |
HDLc (mg/dL) | 44.3 (± 14.8) | 56.5 (±34.3) | <0.001 |
LDLc (mg/dL) | 113.5 (± 47.1) | 65.5 (±44.1) | <0.001 |
Gen | SNP | AA | MAF | ORADD (95% CI), p | ORDOM (95% CI), p | ORREC (95% CI), p |
---|---|---|---|---|---|---|
PSRC1 | rs599839 | G | 0.20 | 0.72 (0.56–0.92), 0.009 | 0.66 (0.49–0.89), 0.007 | 0.70 (0.35–1.38), 0.313 |
MRAS | rs9818870 | T | 0.05 | 0.86 (0.56–1.32), 0.509 | 0.82 (0.53–1.27), 0.383 | - |
BTN2A1 | rs6929846 | T | 0.28 | 0.94 (0.75–1.18), 0.631 | 0.95 (0.71–1.26), 0.735 | 0.87 (0.51–1.47), 0.616 |
MTHFD1L | rs6922269 | A | 0.37 | 1.02 (0.84–1.25), 0.778 | 1.03 (0.78–1.38), 0.791 | 1.03 (0.70–1.53), 0.853 |
CDKN2B | rs1333049 | G | 0.49 | 0.99 (0.81–1.22), 0.997 | 0.91 (0.66–1.27), 0.619 | 1.08 (0.77–1.51), 0.619 |
KIAA1462 | rs3739998 | G | 0.45 | 1.12 (0.92–1.37), 0.248 | 1.09 (0.80–1.48), 0.578 | 1.27 (0.90–1.80), 0.169 |
CXCL12 | rs501120 | C | 0.26 | 0.99 (0.79–1.25), 0.985 | 0.93 (0.69–1.24), 0.640 | 1.26 (0.73–2.16), 0.402 |
HNF1A | rs2259816 | T | 0.41 | 1.22 (0.98–1.52), 0.067 | 1.35 (0.97–1.87), 0.066 | 1.24 (0.83–1.84), 0.286 |
© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
Share and Cite
Rodríguez-Arellano, M.E.; Solares-Tlapechco, J.; Costa-Urrutia, P.; Cárdenas-Hernández, H.; Vallejo-Gómez, M.; Granados, J.; Salas-Padilla, S. Association of the PSRC1 rs599839 Variant with Coronary Artery Disease in a Mexican Population. Medicina 2020, 56, 427. https://doi.org/10.3390/medicina56090427
Rodríguez-Arellano ME, Solares-Tlapechco J, Costa-Urrutia P, Cárdenas-Hernández H, Vallejo-Gómez M, Granados J, Salas-Padilla S. Association of the PSRC1 rs599839 Variant with Coronary Artery Disease in a Mexican Population. Medicina. 2020; 56(9):427. https://doi.org/10.3390/medicina56090427
Chicago/Turabian StyleRodríguez-Arellano, Martha Eunice, Jacqueline Solares-Tlapechco, Paula Costa-Urrutia, Helios Cárdenas-Hernández, Marajael Vallejo-Gómez, Julio Granados, and Sergio Salas-Padilla. 2020. "Association of the PSRC1 rs599839 Variant with Coronary Artery Disease in a Mexican Population" Medicina 56, no. 9: 427. https://doi.org/10.3390/medicina56090427