Balkan Journal of Medical Genetics

THE +3953 (C->T) POLYMORPHISM OF INTERLEUKIN-1β GENE IN MYOCARDIAL INFARCTION IN TATARS AND RUSSIANS FROM BASHKORTOSTAN
Tulyakova G1,*, Nasibullin T1, Zakirova A2, Khusnutdinova E1, Mustafina O1
*Corresponding Author: Dr. Gulnara Tulyakova, Institute of Biochemistry and Genetics, Ufa Research Center, Russian Academy of Sciences, October Avenue 69, 450054 Ufa, Bashkortostan, Russia; Tel.: +7-3472-361176; Fax: +7-3472-356100; E-mail: gulnarat@mail.ru
page: 65

INTRODUCTION

A number of experimental studies support a role for interleukin-1β (IL-1β) in the pathogenesis of atherosclerosis [1-3]. Interleukin-1b is a proinflammatory cytokine with pleiotropic biological effects. It enhances the release of endothelin [4], stimulates activation of macrophages, induces secretion of metalloproteinase-9, and promotes the _expression of both intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in endothelial cell and in vascular smooth muscle cells [5,6]. It is an important co-stimulatory factor for T-cell activation and for the secretion of the proapoptotic cytokine tumor necrosis factor α (TNFα) [6]. Interleukin-1β and TNFα are powerful inhibitors of lipoprotein lipase, that could lead to hypertriglyceridemia [2]. Interleukin-1 can also increase the _expression of genes for fibrinogen, tissue factor, and types 1 and 2 plasminogen activator inhibitor [3]. Interleukin-1b leads to increased production of nitric oxide and of prostaglandin E2 [6,7].

Of the 10 components of the IL-1 gene family, nine map to human chromosome 2q13 [7]. Four genetic polymorphisms have been identified in the IL-1β gene [8], of which one is at position +3953 in exon 5. The T allele of the +3953 (C→T) IL-1β polymorphism is less common than the C allele and is associated with an increased serum IL-1b level [8,9]. The aim of the present study was to assess the genotype and allele frequency of the +3953 (C→T) IL-1b polymorphism in Russians and Tatars from Bashkortostan and to look for a possible association of this polymorphism with myocardial infarction (MI).

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