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Mediators of Inflammation
Volume 2011, Article ID 525691, 6 pages
http://dx.doi.org/10.1155/2011/525691
Clinical Study

CCL5/RANTES Gene Polymorphisms in Slavonic Patients with Myocardial Infarction

1Laboratory of Immunogenomics and Proteomics, Institute of Molecular and Translational Medicine, Palacky University and Faculty Hospital, 775 20 Olomouc, Czech Republic
2Institute of Internal Medicine, Siberian Branch of Russian Academy of Medical Sciences, Novosibirsk 630089, Russia
3Internal Medicine—Cardiology, Palacky University and Faculty Hospital, 775 20 Olomouc, Czech Republic
4Cardiogenetics and Immunogenetics Laboratory, Palacky University and Faculty Hospital, 775 20 Olomouc, Czech Republic

Received 30 November 2010; Accepted 27 January 2011

Academic Editor: Y. Mandi

Copyright © 2011 Irina P. Tereshchenko et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Coronary artery inflammation is a critical process in the pathogenesis of myocardial infarction (MI). The chemokine CCL5/RANTES (regulated upon activation, normal T cells expressed and secreted) is expressed in advanced atherosclerotic lesions. Functional polymorphisms of the RANTES gene can, therefore, be involved in the pathogenesis of coronary artery disease. We examined the association of polymorphisms in the RANTES gene with myocardial infarction in Slavonic populations of Czech and Russian origin. A total of 467 post-MI patients and 337 control subjects were genotyped for RANTES promoter G-403A (rs2107538) and intron 1.1 T/C (rs2280789) variants by PCR-SSP. Both RANTES genotypes and allele frequencies did not differ between case and control groups. Haplotype-based analysis also failed to reveal an association between MI and investigated markers. Strong linkage disequilibrium was detected between particular RANTES alleles. The data do not support an association between RANTES G-403A polymorphism and MI, as reported previously.