Is LOX-1 K167N polymorphism protective for coronary artery disease?
Is LOX-1 K167N polymorphism protective for coronary artery disease?
复制标题
LOX-1 K167N 多态性对冠状动脉疾病有保护作用吗？
作者：
Ozlem Kurnaz;H. Aydogan;C. Isbir;A. Tekeli;T. Isbir
背景
人凝集素样氧化低密度脂蛋白受体1（LOX-1，OLR 1）是血管内皮细胞上氧化低密度脂蛋白（oxLDL）的细胞表面内吞受体。OxLDL被巨噬细胞贪婪地摄取，导致泡沫细胞形成。OxLDL还参与诱导平滑肌细胞迁移、增殖和转化。LOX-1基因的单核苷酸多态性K167 N（G501 C）导致第167位残基的氨基酸二态性（Lys/Asn）。这个赖氨酸残基的替代导致oxLDL的结合和内化减少。本研究的目的是探讨土耳其冠心病（CAD）患者LOX-1 K167 N基因多态性的影响。
材料和方法
应用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）方法，对91例冠心病患者和72例健康对照者的K167 N基因多态性进行了研究。
结果
冠心病组KK基因型和K等位基因频率均高于对照组（p<0.05），对照组NN基因型频率高于冠心病组（p<0.05）。男性（OR：0.400 -->0.481）和吸烟（OR：0.400-->0.949）可逆转携带N等位基因患者CAD风险的降低。虽然男性和吸烟在N等位基因患者中低于其他心血管危险因素，但在K等位基因患者中高于其他心血管危险因素。
结论
男性和吸烟降低了N等位基因的保护作用。K等位基因对K167 N多态性引起的CAD风险的不利影响似乎与其他心血管危险因素无关。
BACKGROUND
Human lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1, OLR1) has been identified as a cell surface endocytosis receptor for oxidized low-density lipoprotein (oxLDL) on vascular endothelial cells. OxLDLs are avidly ingested by macrophages, resulting in foam cell formation. OxLDLs are also involved in inducing smooth muscle cell migration, proliferation and transformation. A single nucleotide polymorphism K167N (G501C) of the LOX-1 gene results in an amino acid dimorphism (Lys/Asn) at residue 167. Replacement of this Lys residue causes reduced binding and internalization of oxLDL. The purpose of this study was to investigate the effect of the LOX-1 K167N gene polymorphism in Turkish patients with coronary artery disease (CAD).
MATERIALS AND METHODS
K167N polymorphism were studied in 91 patients with CAD and 72 healthy controls by the PCR-RFLP method.
RESULTS
The frequencies of the KK genotype and the K allele were higher in the CAD group than the controls (p<0.05), while the frequency of the NN genotype was higher in the control group than in the CAD group (p<0.05). It was observed that the decreased CAD risk in patients who had the N allele was reversed by male sex (OR: 0.400 -->0.481) and smoking (OR: 0.400 -->0.949). Although male sex and smoking were lower than other cardiovascular risk factors in patients with the N allele they were higher than other cardiovascular risk factors in patients with the K allele.
CONCLUSION
Male sex and smoking decrease the protective effects of the N allele. The adverse effects of the K allele on the CAD risk resulting from the K167N polymorphism appear to be independent of other cardiovascular risk factors.
氧化磷脂与氧化 LDL 的载脂蛋白 B 连接，是巨噬细胞清道夫受体的配体。
影响因子：
6.5
作者：
Gillotte,KL;Hörkkö,S;Witztum,JL;Steinberg,D
通讯作者：
Steinberg,D