PECAM-1 GENE POLYMORPHISM (rs668) AND SUBCLINICAL MARKERS OF CAROTID ATHEROSCLEROSIS IN PATIENTS WITH TYPE 2 DIABETES MELLITUS
Popović D, Nikolajević Starčević J, Šantl Letonja M, Makuc J, Cokan Vujkovac A, Reschner H, Bregar D, Petrovič D
*Corresponding Author: Professor Daniel Petrovič, M.D., Ph.D., Institute of Histology and Embryology, Faculty of Medicine University Ljubljana, Korytkova 2, SI-1000 Ljubljana, Slovenia. Tel: +386-1-543-7367. Fax: +386-1-543-7361. E-mail: daniel.petrovic@mf.uni-lj.si
page: 63

INTRODUCTION

The leukocyte adhesion and their transendothelial migration play an important role in the initial phase of atherogenesis [1]. Processes are regulated by various types of adhesion molecules, such as platelet endothelial cell adhesion molecule 1 (PECAM-1), intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1). The plasma level of adhesion molecules is elevated in individuals with atherosclerosis [2-4]. Platelet endothelial cell adhesion molecule 1, also called CD31, is a 130 kD member of the immunoglobulin superfamily, consisting of six extracellular immunoglo-bulin-like domains, one transmembrane domain, and one cytoplasmic domain. Their expression takes place on the surface of circulating platelets, monocytes, neutrophils and selected T cells [5,6]. The PECAM-1 is a signaling molecule that plays diverse roles in vascular biology, including modulation of platelet function [7,8], angiogenesis [9], vasculogenesis [10], integrin regulation [11], T-cell and B-cell activation [12] and mediation of leukocyte migration across the endothelium [13]. The PECAM-1 gene is located at the end of the long arm of the chromosome 17 (17q23). Previous studies have reported the existence of 11 different single nucleotide polymorphisms (SNPs) of the PECAM-1 gene. Three of them have been described that encode amino acid substitutions in the PECAM-1 molecule. A mutation in the PECAM-1 gene in exon 3 at position +373 involves a C>G substitution, causing a leucine to valine substitution at position 125 (rs668) [14]. The interaction or activation of the PECAM-1 take place via homophilic binding with its first extracellular Ig-like domains [15,16]. This polymorphism might affect the homophilic binding capability and influence individual susceptibility to the development of atherosclerosis. The association between the rs668 PECAM-1 polymorphism and cardiovascular disease was studied in Caucasians [17-19], Japanese [20] and Chinese [21], but no clear answer on the association between the rs668 polymorphism of PECAM-1 and the development of cardiovascular diseases could be provided. Platelet endothelial cell adhesion molecule 1 is important in the detection of mechanoreception (mechanical shear force) and mechanotransduction (conversion into chemical signals) by the endothelium [22,23]. Atherosclerotic lesion development occurs at sites of the vessel where flow and shear stress conditions are disturbed [24]. Pulsatile or oscillatory shear stresses induce pro inflammatory gene expression [25]. Using the mouse model, the effect of PECAM-1 deficiency (double knock-out mice model without the presence of the PECAM-1 gene) on the development of atherosclerosis. They reported reduced atherosclerotic lesions in double knock-out mice models [21,25]. The purpose of this study was to investigate an association between the rs668 (+373C/G) polymorphism of the PECAM-1 gene and subclinical markers of carotid atherosclerosis in patients with type 2 diabetes mellitus (T2DM).



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