A variant in the ABO gene explains the variation in soluble E-selectin levels-results from dense genotyping in two independent populations

PLoS One. 2012;7(12):e51441. doi: 10.1371/journal.pone.0051441. Epub 2012 Dec 28.

Abstract

Background: Elevated soluble (s) E-selectin levels have been associated with various cardiovascular diseases. Recently, genetic variants in the ABO blood group have been related to E-selectin levels in a small cohort of patients with type 1 diabetes. We evaluated whether this association is reproducible in two large samples of Caucasians.

Methodology/ principal findings: Data of the present study was drawn from the population-based MONICA/KORA Augsburg study (n = 1,482) and the patients-based LURIC study (n = 1,546). A high-density genotyping array (50K IBC Chip) containing single-nucleotide polymorphisms (SNPs) from E-selectin candidate genes selected on known biology of E-selectin metabolism, mouse genetic studies, and human genetic association studies, was used for genotyping. Linear regression analyses with adjustment for age and sex (and survey in KORA) were applied to assess associations between gene variants and sE-selectin concentrations. A number of 12 SNPs (in KORA) and 13 SNPs (in LURIC), all from the ABO blood group gene, were significantly associated with the log-transformed concentration of E-selectin. The strongest association was observed for rs651007 with a change of log-transformed sE-selectin per one copy of the minor allele of -0.37 ng/ml (p = 1.87×10(-103)) in KORA and -0.35 ng/ml (p = 5.11×10(-84)) in LURIC. Inclusion of rs651007 increased the explained sE-selectin variance by 0.256 in KORA and 0.213 in LURIC. All SNPs had minor allele frequencies above 20% showing a substantial gene variation.

Conclusions/ significance: Our findings in two independent samples indicate that the genetic variants at the ABO locus affect sE-selectin levels. Since distinct genome-wide association studies linked the ABO gene with myocardial infarction (MI) in the presence of coronary atherosclerosis and with coronary artery disease, these findings may not only enhance our understanding of adhesion molecule biology, but may also provide a focus for several novel research avenues.

Publication types

  • Multicenter Study
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • ABO Blood-Group System / genetics*
  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Animals
  • Cardiovascular Diseases / epidemiology
  • Cardiovascular Diseases / etiology*
  • Disease Models, Animal
  • E-Selectin / genetics*
  • Female
  • Genetic Predisposition to Disease*
  • Genome-Wide Association Study*
  • Genotype
  • Germany / epidemiology
  • Humans
  • Male
  • Mice
  • Middle Aged
  • Phenotype
  • Polymorphism, Single Nucleotide / genetics*
  • Risk Factors
  • Young Adult

Substances

  • ABO Blood-Group System
  • E-Selectin

Grants and funding

The MONICA/KORA Augsburg studies were financed by the Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany and supported by grants from the German Federal Ministry of Education and Research (BMBF). Part of this work was financed by the German National Genome Research Network (NGFNPlus, project number 01GS0834), by the German Research Foundation (TH-784/2-1 and TH-784/2-2), by the European Foundation for the Study of Diabetes and through additional funds from the Helmholtz Zentrum München, the German Diabetes Center and the University of Ulm. Furthermore, the research was supported within the Munich Center of Health Sciences (MC Health) as part of the Ludwig Maximilians University (LMU) innovative. LURIC received funding through the 6th Framework Programme (integrated project Bloodomics, grant LSHM-CT-2004-503485) and the 7th of Framework Programme (integrated project AtheroRemo, Grant Agreement number 201668) of the European Union. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.