title: Is LOX-1 K167N polymorphism protective for coronary artery disease?
abstract: 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).
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institute of Experimental Medicine, Department of Molecular Medicine, Istanbul University, Istanbul, Turkey.
authors.forename: Ozlem
authors.initials: O
authors.lastname: Kurnaz
authors.forename: Hülya Yilmaz
authors.initials: HY
authors.lastname: Aydogan
authors.forename: C Selim
authors.initials: CS
authors.lastname: Isbir
authors.forename: Atike
authors.initials: A
authors.lastname: Tekeli
authors.forename: Turgay
authors.initials: T
authors.lastname: Isbir
mesh_terms: D003324:Coronary Artery Disease / Q000453:epidemiology / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D017720:Molecular Epidemiology; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide; D051127:Scavenger Receptors, Class E / Q000235:genetics* / Q000378:metabolism; D012907:Smoking; D014421:Turkey / Q000453:epidemiology
chemical_list: C495137:OLR1 protein, human; D051127:Scavenger Receptors, Class E