The (G > A) rs11573191 polymorphism of PLA2G5 gene is associated with premature coronary artery disease in the mexican mestizo population: The genetics of atherosclerotic disease Mexican study
Por:
Vargas-Alarcón G., Posadas-Romero C., Villarreal-Molina T., Alvarez-León E., Angeles-Martinez J., Soto M.E., Monroy-Muñoz I., Juárez J.G., Sánchez-Ramírez C.J., Ramirez-Bello J., Ramírez-Fuentes S., Fragoso J.M., Rodríguez-Pérez J.M.
Publicada:
1 ene 2014
Resumen:
Coronary artery disease (CAD) is a multifactorial disorder that results from an excessive inflammatory response. Secretory phospholipase A2-V (sPLA2-V) encoded by PLA2G5 gene promotes diverse proinflammatory processes. The aim of the present study was to analyze if PLA2G5 gene polymorphisms are associated with premature CAD. Three PLA2G5 polymorphisms (rs11573187, rs2148911, and rs11573191) were analyzed in 707 patients with premature CAD and 749 healthy controls. Haplotypes were constructed after linkage disequilibrium analysis. Under dominant, recessive, and additive models, the rs11573191 polymorphism was associated with increased risk of premature CAD (OR = 1.51, P dom = 3.5 × 10-3; OR = 2.95, P rec = 0.023; OR = 1.51, P add = 1.2 × 10 -3). According to the informatics software, this polymorphism had a functional effect modifying the affinity of the sequence by the MZF1 transcription factor. PLA2G5 polymorphisms were in linkage disequilibrium and the CGA haplotype was associated with increased risk of premature CAD (OR = 1.49, P = 0.0023) and with hypertension in these patients (OR = 1.75, P = 0.0072). Our results demonstrate the association of the PLA2G5 rs11573191 polymorphism with premature CAD. In our study, it was possible to distinguish one haplotype associated with increased risk of premature CAD and hypertension. © 2014 Gilberto Vargas-Alarcón et al.
Filiaciones:
Vargas-Alarcón G.:
Department of Molecular Biology, Endocrinology, and Immunology, National Institute of Cardiology Ignacio Chávez, 14080 Mexico City, DF, Mexico
Posadas-Romero C.:
Department of Endocrinology, National Institute of Cardiology Ignacio Chávez, Juan Badiano 1, Sección XVI, Tlalpan, 14080 Mexico City, DF, Mexico
Villarreal-Molina T.:
Cardiovascular Genomics Laboratory, National Institute of Genomic Medicine, 14610 Mexico City, DF, Mexico
Alvarez-León E.:
Department of Molecular Biology, Endocrinology, and Immunology, National Institute of Cardiology Ignacio Chávez, 14080 Mexico City, DF, Mexico
Angeles-Martinez J.:
Department of Molecular Biology, Endocrinology, and Immunology, National Institute of Cardiology Ignacio Chávez, 14080 Mexico City, DF, Mexico
Soto M.E.:
Department of Immunology, National Institute of Cardiology Ignacio Chávez, Juan Badiano 1, Sección XVI, Tlalpan, 14080 Mexico City, DF, Mexico
Monroy-Muñoz I.:
Department of Molecular Biology, Endocrinology, and Immunology, National Institute of Cardiology Ignacio Chávez, 14080 Mexico City, DF, Mexico
Juárez J.G.:
Department of Endocrinology, National Institute of Cardiology Ignacio Chávez, Juan Badiano 1, Sección XVI, Tlalpan, 14080 Mexico City, DF, Mexico
Sánchez-Ramírez C.J.:
Department of Molecular Biology, Endocrinology, and Immunology, National Institute of Cardiology Ignacio Chávez, 14080 Mexico City, DF, Mexico
Ramirez-Bello J.:
Laboratory of Genomic Medicine, Research Unit, Juárez de México Hospital, 07760 Mexico City, DF, Mexico
Ramírez-Fuentes S.:
Department of Molecular Biology, Endocrinology, and Immunology, National Institute of Cardiology Ignacio Chávez, 14080 Mexico City, DF, Mexico
Fragoso J.M.:
Department of Molecular Biology, Endocrinology, and Immunology, National Institute of Cardiology Ignacio Chávez, 14080 Mexico City, DF, Mexico
Rodríguez-Pérez J.M.:
Department of Molecular Biology, Endocrinology, and Immunology, National Institute of Cardiology Ignacio Chávez, 14080 Mexico City, DF, Mexico
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