BACKGROUND AND AIM: Oxidized low-density lipoproteins (OxLDLs) play a critical role in endothelial dysfunction, which is implicated in the pathogenesis of atherosclerosis. Vascular endothelial 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, hyperlipidemia, 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 OLR1 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.
BACKGROUND AND AIM: Oxidized low-density lipoproteins (OxLDLs) play a critical role in endothelial dysfunction, which is implicated in the pathogenesis of atherosclerosis. Vascular endothelial 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, hyperlipidemia, 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 OLR1 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.
Authors: Tina E Brinkley; Noriaki Kume; Hirokazu Mitsuoka; Michael D Brown; Dana A Phares; Robert E Ferrell; Toru Kita; James M Hagberg Journal: Exp Physiol Date: 2008-05-09 Impact factor: 2.969
Authors: Joshua W Knowles; Themistocles L Assimes; Eric Boerwinkle; Stephen P Fortmann; Alan Go; Megan L Grove; Mark Hlatky; Carlos Iribarren; Jun Li; Richard Myers; Neil Risch; Stephen Sidney; Audrey Southwick; Kelly A Volcik; Thomas Quertermous Journal: BMC Med Genet Date: 2008-04-02 Impact factor: 2.103