Variation in the selenoprotein S gene locus is associated with coronary heart disease and ischemic stroke in two independent Finnish cohorts |
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Authors: | Mervi Alanne Kati Kristiansson Kirsi Auro Kaisa Silander Kari Kuulasmaa Leena Peltonen Veikko Salomaa Markus Perola |
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Institution: | (1) Department of Molecular Medicine, KTL-National Public Health Institute, Biomedicum, P.O. Box 104, 00251 Helsinki, Finland;(2) Department of Molecular Medicine, KTL-National Public Health Institute, Helsinki, Finland;(3) Department of Health Promotion and Chronic Disease Prevention, KTL-National Public Health Institute, Helsinki, Finland;(4) Faculty of Medicine, Department of Medical Genetics, University of Helsinki, Helsinki, Finland;(5) The Broad Institute, Massachusetts Institute of Technology, Boston, MA, USA |
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Abstract: | Selenoprotein S (SEPS1) is a novel candidate gene involved in the regulation of inflammatory response and protection from
oxidative damage. This study explored the genetic variation in the SEPS1 locus for an association with CVD as well as with
quantitative phenotypes related to obesity and inflammation. We used the case-cohort design and time-to-event analysis in
two separate prospectively followed population-based cohorts FINRISK 92 and 97 (n = 999 and 1,223 individuals, respectively) to study the associations of five single nucleotide polymorphisms with the risk
for coronary heart disease (CHD) and ischemic stroke events. We found a significant association with increased CHD risk in
females carrying the minor allele of rs8025174 in the combined analysis of both cohorts hazard ratio (HR) 2.95 (95% confidence interval: 1.37–6.39)]. Another variant,
rs7178239, increased the risk for ischemic stroke significantly in females HR: 3.35 (1.66–6.76)] and in joint analysis of both sexes
and both cohorts HR: 1.75 (1.17–2.64)]. These results indicate that variation in the SEPS1 locus may have an effect on CVD
morbidity, especially in females. This observation should stimulate further investigations of the role of this gene and protein
in the pathogenesis of CVD.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. |
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