title: [Increased lectin-like oxidized low density lipoprotein receptor-1 expression in the autologous vein grafts and vein graft atherosclerosis].
abstract: OBJECTIVE
  To study the changes of lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) expression in the autologous vein grafts and vein graft atherosclerotic lesions.
  
  
  METHODS
  Thirty New Zealand white rabbits were randomly assigned to normal control group (rabbits fed with normal diet, n = 10), vein graft group (autologous external jugular vein grafting to common carotid artery and fed with normal diet, n = 10) or vein graft plus high-lipid diet group (autologous vein graft and fed with high-lipid diet, n = 10) for 12 weeks. LOX-1 expressions in the grafts were examined by immunohistochemistry and semi-quantitative reverse transcription-PCR. The relationships between serum total cholesterol level, intimal thickness and LOX-1 expression were also investigated.
  
  
  RESULTS
  LOX-1 expression was low in the endothelium of external jugular veins in the normal control group and significantly increased in the endothelium and neointima of vein grafts in the vein graft group (0.31 +/- 0.14 vs. 0.09 +/- 0.04, P < 0.01) and which was further increased in the endothelium and atherosclerotic lesions in the vein graft plus high-lipid diet group (0.93 +/- 0.34 vs. 0.31 +/- 0.14, P < 0.01). LOX-1 expression in the atherosclerotic lesions was located both in endothelial cells and foam cells and the expression was most prominent in endothelial cells. LOX-1 expression and intimal thickness were positively related to serum total cholesterol level (P = 0.00 and 0.02) and the partial correlation coefficient was 0.78 and 0.42, respectively.
  
  
  CONCLUSIONS
  LOX-1 expression is increased in endothelium and neointima of autologous vein grafts of rabbits. Hypercholesterolemia upregulates LOX-1 expression in vein graft atherosclerosis. Thus, LOX-1 might play an important role in the pathogenesis of vein graft atherosclerosis.
authors.affiliation: Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
authors.forename: Dong
authors.initials: D
authors.lastname: Huang
authors.forename: Jun-bo
authors.initials: JB
authors.lastname: Ge
authors.forename: Chun
authors.initials: C
authors.lastname: Liang
authors.forename: Yu-kun
authors.initials: YK
authors.lastname: Luo
authors.forename: Qing-zhe
authors.initials: QZ
authors.lastname: Jia
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D006083:Graft Occlusion, Vascular / Q000378:metabolism* / Q000473:pathology; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D011817:Rabbits; D051127:Scavenger Receptors, Class E / Q000378:metabolism*; D014182:Transplantation, Autologous; D014680:Veins / Q000637:transplantation
chemical_list: D008077:Lipoproteins, LDL; D051127:Scavenger Receptors, Class E