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CASP1 Gene Polymorphisms and BAT1-NFKBIL-LTA-CASP1 Gene–Gene Interactions Are Associated with Restenosis after Coronary Stenting

In the present study, we evaluated the association of the BAT1, NFKBIL, LTA, and CASP1 single nucleotide polymorphisms and the gene–gene interactions with risk of developing restenosis after coronary stenting. The allele and genotype determination of the polymorphisms (BAT1 rs2239527 C/G, NFKBIL1 rs...

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Autores principales: Vargas-Alarcón, Gilberto, Ramírez-Bello, Julian, Peña-Duque, Marco Antonio, Martínez-Ríos, Marco Antonio, Delgadillo-Rodríguez, Hilda, Fragoso, José Manuel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9221501/
https://www.ncbi.nlm.nih.gov/pubmed/35740890
http://dx.doi.org/10.3390/biom12060765
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author Vargas-Alarcón, Gilberto
Ramírez-Bello, Julian
Peña-Duque, Marco Antonio
Martínez-Ríos, Marco Antonio
Delgadillo-Rodríguez, Hilda
Fragoso, José Manuel
author_facet Vargas-Alarcón, Gilberto
Ramírez-Bello, Julian
Peña-Duque, Marco Antonio
Martínez-Ríos, Marco Antonio
Delgadillo-Rodríguez, Hilda
Fragoso, José Manuel
author_sort Vargas-Alarcón, Gilberto
collection PubMed
description In the present study, we evaluated the association of the BAT1, NFKBIL, LTA, and CASP1 single nucleotide polymorphisms and the gene–gene interactions with risk of developing restenosis after coronary stenting. The allele and genotype determination of the polymorphisms (BAT1 rs2239527 C/G, NFKBIL1 rs2071592 T/A, LTA rs1800683 G/A, CASP1 rs501192 A/G, and CASP1 rs580253 A/G) were performed by 5’exonuclease TaqMan assays in 219 patients: 66 patients with restenosis and 153 without restenosis. The distribution of rs2239527 C/G, rs2071592 T/A, and rs1800683 G/A polymorphisms was similar in patients with and without restenosis. Nonetheless, under recessive (OR = 2.73, pC(Res) = 0.031) and additive models (OR = 1.65, pC(Add) = 0.039), the AA genotype of the rs501192 A/G polymorphism increased the restenosis risk. Under co-dominant, dominant, recessive, and additive models, the AA genotype of the rs580253 A/G was associated with a high restenosis risk (OR = 5.38, pC(Co-Dom) = 0.003; OR = 2.12, pC(Dom) = 0.031; OR = 4.32, pC(Res) = 0.001; and OR = 2.16, 95%CI: 1.33–3.52, pC(Add) = 0.001, respectively). In addition, we identified an interaction associated with restenosis susceptibility: BAT1-NFKBIL1-LTA-CASP1 (OR = 9.92, p < 0.001). In summary, our findings demonstrate that the rs501192 A/G and rs580253 A/G polymorphisms, as well as the gene–gene interactions between BAT1-NFKBIL1-LTA-CASP1, are associated with an increased restenosis risk after coronary stenting.
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spelling pubmed-92215012022-06-24 CASP1 Gene Polymorphisms and BAT1-NFKBIL-LTA-CASP1 Gene–Gene Interactions Are Associated with Restenosis after Coronary Stenting Vargas-Alarcón, Gilberto Ramírez-Bello, Julian Peña-Duque, Marco Antonio Martínez-Ríos, Marco Antonio Delgadillo-Rodríguez, Hilda Fragoso, José Manuel Biomolecules Article In the present study, we evaluated the association of the BAT1, NFKBIL, LTA, and CASP1 single nucleotide polymorphisms and the gene–gene interactions with risk of developing restenosis after coronary stenting. The allele and genotype determination of the polymorphisms (BAT1 rs2239527 C/G, NFKBIL1 rs2071592 T/A, LTA rs1800683 G/A, CASP1 rs501192 A/G, and CASP1 rs580253 A/G) were performed by 5’exonuclease TaqMan assays in 219 patients: 66 patients with restenosis and 153 without restenosis. The distribution of rs2239527 C/G, rs2071592 T/A, and rs1800683 G/A polymorphisms was similar in patients with and without restenosis. Nonetheless, under recessive (OR = 2.73, pC(Res) = 0.031) and additive models (OR = 1.65, pC(Add) = 0.039), the AA genotype of the rs501192 A/G polymorphism increased the restenosis risk. Under co-dominant, dominant, recessive, and additive models, the AA genotype of the rs580253 A/G was associated with a high restenosis risk (OR = 5.38, pC(Co-Dom) = 0.003; OR = 2.12, pC(Dom) = 0.031; OR = 4.32, pC(Res) = 0.001; and OR = 2.16, 95%CI: 1.33–3.52, pC(Add) = 0.001, respectively). In addition, we identified an interaction associated with restenosis susceptibility: BAT1-NFKBIL1-LTA-CASP1 (OR = 9.92, p < 0.001). In summary, our findings demonstrate that the rs501192 A/G and rs580253 A/G polymorphisms, as well as the gene–gene interactions between BAT1-NFKBIL1-LTA-CASP1, are associated with an increased restenosis risk after coronary stenting. MDPI 2022-05-31 /pmc/articles/PMC9221501/ /pubmed/35740890 http://dx.doi.org/10.3390/biom12060765 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Vargas-Alarcón, Gilberto
Ramírez-Bello, Julian
Peña-Duque, Marco Antonio
Martínez-Ríos, Marco Antonio
Delgadillo-Rodríguez, Hilda
Fragoso, José Manuel
CASP1 Gene Polymorphisms and BAT1-NFKBIL-LTA-CASP1 Gene–Gene Interactions Are Associated with Restenosis after Coronary Stenting
title CASP1 Gene Polymorphisms and BAT1-NFKBIL-LTA-CASP1 Gene–Gene Interactions Are Associated with Restenosis after Coronary Stenting
title_full CASP1 Gene Polymorphisms and BAT1-NFKBIL-LTA-CASP1 Gene–Gene Interactions Are Associated with Restenosis after Coronary Stenting
title_fullStr CASP1 Gene Polymorphisms and BAT1-NFKBIL-LTA-CASP1 Gene–Gene Interactions Are Associated with Restenosis after Coronary Stenting
title_full_unstemmed CASP1 Gene Polymorphisms and BAT1-NFKBIL-LTA-CASP1 Gene–Gene Interactions Are Associated with Restenosis after Coronary Stenting
title_short CASP1 Gene Polymorphisms and BAT1-NFKBIL-LTA-CASP1 Gene–Gene Interactions Are Associated with Restenosis after Coronary Stenting
title_sort casp1 gene polymorphisms and bat1-nfkbil-lta-casp1 gene–gene interactions are associated with restenosis after coronary stenting
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9221501/
https://www.ncbi.nlm.nih.gov/pubmed/35740890
http://dx.doi.org/10.3390/biom12060765
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