Influence of haplotypes, gene expression and soluble levels of L-selectin on the risk of acute coronary syndrome

L-selectin gene (SELL) is a candidate gene for the development of acute coronary syndrome (ACS) that contributes to endothelial dysfunction. The −642C>T (rs2205849) and 725C>T (rs2229569) polymorphisms have been associated with changes in gene expression, ligand affinity and increased risk of...

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Veröffentlicht in:Gene 2017-08, Vol.625, p.31-41
Hauptverfasser: Sandoval-Pinto, Elena, Padilla-Gutiérrez, Jorge Ramón, Hernández-Bello, Jorge, Martínez-Fernández, Diana Emilia, Valdés-Alvarado, Emmanuel, Muñoz-Valle, José Francisco, Flores-Salinas, H.E., Valle, Yeminia
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Sprache:eng
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Zusammenfassung:L-selectin gene (SELL) is a candidate gene for the development of acute coronary syndrome (ACS) that contributes to endothelial dysfunction. The −642C>T (rs2205849) and 725C>T (rs2229569) polymorphisms have been associated with changes in gene expression, ligand affinity and increased risk of cardiovascular disease. The aim of this study was to investigate the association between the haplotypes constructed with the −642C>T and 725C>T polymorphisms of the SELL gene, the expression levels of its mRNA and the serum levels of soluble L-selectin with ACS. We recruited 615 individuals of Mexican origin matched by age, including 342 patients with ACS and 273 individuals without personal history of ischemic cardiopathy as control group (CG). Genotyping was performed by PCR-RFLP. The qPCR technique was used to analyze the expression of mRNA using TaqMan® UPL probes. The levels of soluble L-selectin were measured with ELISA. The allele variants in both polymorphisms were over-represented in the CG compared to the ACS (OR range: 0.371–0.716, pT SELL polymorphisms are protective factors against ACS.•SELL gene expression was increased in ACS patients.•Both polymorphisms had no effect on mRNA expression and soluble protein levels.•sL-selectin levels seem to be affected by age and gender in Western Mexico
ISSN:0378-1119
1879-0038
DOI:10.1016/j.gene.2017.05.005