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      Association of the Phe206Leu Allele of the L-Selectin Gene with Coronary Artery Disease


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          Background and Aims: The aim of this study was to assess the association between the L-selectin Phe206Leu polymorphism and coronary artery disease. Methods: A total of 322 patients (221 men and 101 women) with coronary artery disease in one or more vessels documented by angiography were studied; 157 subjects (85 men and 72 women) without atherosclerosis were included as controls. All subjects were genotyped for the L-selectin Phe206Leu gene polymorphism using polymerase chain reaction with sequence-specific primer (PCR-SSP). To assess disease severity, all patients were classified by numbers of coronary arteries with 50% stenosis. Results: A significantly increased frequency of the 206Leu mutant allele was observed in patients with coronary artery disease compared to the controls. The 206Leu allele frequency occurred in 42% of the patients with coronary artery disease compared to 30% of the controls (p < 0.009). No association was found between the severity of coronary artery disease and the L-selectin Phe206Leu polymorphism. Conclusion: Our findings suggest that carriage of L-selectin 206Leu mutant allele could contribute to susceptibility of Iranian individuals to contracting coronary artery disease.

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          Most cited references 21

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          Site specificity of atherosclerosis: site-selective responses to atherosclerotic modulators.

          Atherosclerosis is a complex disease process that affects very specific sites of the vasculature. It is recognized that hemodynamic forces are largely responsible for dictating which vascular sites are either susceptible or resistant to developing atherosclerosis. In addition, a number of systemic and local factors also modulate the pathogenesis of the disease. By studying the development of atherosclerosis in mice, investigators have gained insights into the molecular mechanisms of this disease, although studies have largely focused on a single vascular site. Here, we review those recent studies in which vascular site-specific effects on atherosclerosis were reported when more than 1 site was examined. We assess the hypothesis that regional differences in the hemodynamic profile prime the endothelial phenotype to respond distinctly to such systemic risk factors as hypercholesterolemia, genetics, immune status, gender, and oxidative stress. Because a given treatment may differentially affect the development of atherosclerotic lesions throughout the vasculature, the sites chosen for study are critically important. By accounting for the complex interplay of factors that may operate at these different sites, a more complete understanding of the overriding mechanisms that control the initiation and progression of the atherosclerotic lesion may be realized.
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              Monocyte rolling, arrest and spreading on IL-4-activated vascular endothelium under flow is mediated via sequential action of L-selectin, beta 1-integrins, and beta 2-integrins

              Leukocyte interactions with vascular endothelium at sites of inflammation can be dynamically regulated by activation-dependent adhesion molecules. Current models, primarily based on studies with polymorphonuclear leukocytes, suggest the involvement of multiple members of the selectin, integrin, and immunoglobulin gene families, sequentially, in the process of initial attachment (rolling), stable adhesion (arrest), spreading and ultimate diapedesis. In the current study, IL-4-activated human umbilical vein endothelium, which selectively expresses VCAM-1 and an L-selectin ligand but not E- selectin, and appropriate function blocking monoclonal antibodies, were used to study monocyte-endothelial interactions in an in vitro model that mimics microcirculatory flow conditions. In this system, L- selectin mediates monocyte rolling and also facilitates alpha 4 beta 1- integrin-dependent arrest, whereas beta 2-integrins are required for spreading of firmly attached monocytes on the endothelial cell surface but not their arrest. These findings provide the first in vitro evidence for human monocyte rolling on cytokine-activated endothelium, and suggest a sequential requirement for both beta 1- and beta 2- integrin-dependent adhesive mechanisms in monocyte-endothelial interactions.

                Author and article information

                S. Karger AG
                February 2006
                10 February 2006
                : 105
                : 2
                : 113-118
                Departments of Immunology, aMolecular Medicine Research Center, Hamedan University of Medical Sciences, Hamedan, bIran University of Medical Sciences and cTehran University of Medical Sciences, Tehran, and dDepartment of Cardiology, Tehran University of Medical Sciences, Tehran, Iran; eDepartment of Internal Medicine, University of Texas-Houston, Houston, Tex., USA
                90212 Cardiology 2006;105:113–118
                © 2006 S. Karger AG, Basel

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                Page count
                Tables: 3, References: 32, Pages: 6
                Original Research


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