Background and aim: Oxidized low-density tipoproteins (OxLDLs) play a critical rote in endothetiat dysfunction, which is implicated in the pathogenesis of atherosclerosis. Vascular enclothelial cells internalize and degrade oxLDL through the endothelial lectin-like oxidized LDL receptor 1 (OLR1). OLR1 is up-regulated in several pathological conditions, including hypertension, hyperlipidernia, diabetes, atherosclerosis and inflammation, and represents therefore a good candidate for coronary artery disease (CAD). Recently, a 3'-UTR (188 C > T) SNP in the OLR1 gene has been reported to be associated with coronary artery stenosis and myocardial infarction. In the present study we investigated whether the OLRI gene 188 C > T SNP is a genetic risk marker for CAD in Italian patients with angiographically defined coronary atherosclerosis, and assessed its relation with clinical and metabolic abnormalities, including severity of disease (classified as restenosis, single- or multiple coronary vessels disease, and MI). Methods: The 3'-UTR C > T SNP was detected in real-time PCR in 351 subjects with CAD and in 215 control subjects. Results: The OLR1-T allele frequencies were 48.9% in the CAD subjects and 47.7% in controls, with no significant difference between the two groups. Also, the 3'-UTR C > T SNP did not associate with any of the parameters of severity of disease. Furthermore, none of the other clinical and metabolic parameters were associated with the OLR1 gene SNP. Conclusions: Our observations suggest that, in our population, the 3'-UTR C > T polymorphism of the OLR1 gene is unlikely to play a role in the pathogenesis of coronary artery disease. (c) 2005 Elsevier B.V. All rights reserved.

The 3'-UTR C>T polymorphism of the oxidized LDL-receptor 1 (OLR1) gene does not associate with coronary artery disease in Italian CAD patients or with the severity of coronary disease

BARONI MG
2006-01-01

Abstract

Background and aim: Oxidized low-density tipoproteins (OxLDLs) play a critical rote in endothetiat dysfunction, which is implicated in the pathogenesis of atherosclerosis. Vascular enclothelial cells internalize and degrade oxLDL through the endothelial lectin-like oxidized LDL receptor 1 (OLR1). OLR1 is up-regulated in several pathological conditions, including hypertension, hyperlipidernia, diabetes, atherosclerosis and inflammation, and represents therefore a good candidate for coronary artery disease (CAD). Recently, a 3'-UTR (188 C > T) SNP in the OLR1 gene has been reported to be associated with coronary artery stenosis and myocardial infarction. In the present study we investigated whether the OLRI gene 188 C > T SNP is a genetic risk marker for CAD in Italian patients with angiographically defined coronary atherosclerosis, and assessed its relation with clinical and metabolic abnormalities, including severity of disease (classified as restenosis, single- or multiple coronary vessels disease, and MI). Methods: The 3'-UTR C > T SNP was detected in real-time PCR in 351 subjects with CAD and in 215 control subjects. Results: The OLR1-T allele frequencies were 48.9% in the CAD subjects and 47.7% in controls, with no significant difference between the two groups. Also, the 3'-UTR C > T SNP did not associate with any of the parameters of severity of disease. Furthermore, none of the other clinical and metabolic parameters were associated with the OLR1 gene SNP. Conclusions: Our observations suggest that, in our population, the 3'-UTR C > T polymorphism of the OLR1 gene is unlikely to play a role in the pathogenesis of coronary artery disease. (c) 2005 Elsevier B.V. All rights reserved.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11697/143075
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