title: Polymorphisms in the SAA1/2 gene are associated with carotid intima media thickness in healthy Han Chinese subjects: the Cardiovascular Risk Survey.
abstract: BACKGROUND
  Serum amyloid A protein (SAA) is not only an inflammatory factor, but also an apolipoprotein that can replace apolipoprotein A1 (apoA1) as the major apolipoprotein of high-density lipoprotein (HDL), which has been linked to atherosclerosis. However, the relationship between genetic polymorphisms of SAA and the intima-media thickness (IMT) of the common carotid artery in healthy subjects remains unclear. We investigated the role of SAA1 and SAA2 gene polymorphisms with IMT in a cohort of healthy subjects participating in the Cardiovascular Risk Survey (CRS) study.
  
  
  RESULTS
  Anthropometric and B-mode ultrasound of the carotid IMT were measured in 1914 subjects (849 men; 1065 women) recruited from seven cities in Xinjiang province, (western China). Four SNPs (rs12218, rs2229338, rs1059559, and rs2468844) were genotyped by use of the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The SNP rs12218 was associated with carotid IMT by analyses of a dominate model (P<0.001) and additive model (P = 0.003), and the difference remained significant after multivariate adjustment (P = 0.008, P<0.001, respectively). This relationship was also observed in rs2468844 after multivariate adjustment by recessive model analysis (P = 0.011) but this was not observed in rs2229338 and rs1059559 before and after multivariate adjustment. These associations were not modified by serum HDL concentration. Furthermore, there were significant interactions between rs2468844 and rs12218 (interaction P<0.001) and rs2229338 (interaction P = 0.001) on carotid IMT.
  
  
  CONCLUSIONS
  Both rs12218 of the SAA1 gene and rs2468844 of SAA2 gene are associated with carotid IMT in healthy Han Chinese subjects.
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
authors.forename: Xiang
authors.initials: X
authors.lastname: Xie
authors.forename: Yi-Tong
authors.initials: YT
authors.lastname: Ma
authors.forename: Yi-Ning
authors.initials: YN
authors.lastname: Yang
authors.forename: Zhen-Yan
authors.initials: ZY
authors.lastname: Fu
authors.forename: Xiao-Mei
authors.initials: XM
authors.lastname: Li
authors.forename: Ding
authors.initials: D
authors.lastname: Huang
authors.forename: Xiang
authors.initials: X
authors.lastname: Ma
authors.forename: Bang-Dang
authors.initials: BD
authors.lastname: Chen
authors.forename: Fen
authors.initials: F
authors.lastname: Liu
mesh_terms: D000328:Adult; D044466:Asian People / Q000235:genetics; D002318:Cardiovascular Diseases / Q000097:blood / Q000175:diagnosis / Q000235:genetics; D002339:Carotid Arteries / Q000033:anatomy & histology; D002681:China; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006306:Health Surveys; D006801:Humans; D016014:Linear Models; D015810:Linkage Disequilibrium; D008075:Lipoproteins, HDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide; D012307:Risk Factors; D000685:Serum Amyloid A Protein / Q000235:genetics*; D017540:Tunica Media / Q000033:anatomy & histology*
chemical_list: D008075:Lipoproteins, HDL; C521404:SAA1 protein, human; C083772:SAA2 protein, human; D000685:Serum Amyloid A Protein