title: Elevated plasma level of soluble F11 receptor/junctional adhesion molecule-A (F11R/JAM-A) in hypertension.
abstract: BACKGROUND
  The F11 receptor (F11R, also known as junctional adhesion molecule A (JAM-A)) plays a role in the development of hypertension in rat. Genetic variants in the human F11R gene were demonstrated to influence systolic blood pressure. In the present study, we investigated the relationship between F11R and hypertension by examining the levels of a circulating soluble form of F11R (sF11R) in hypertensive patients.
  
  
  METHODS
  Plasma sF11R was measured by enzyme-linked immunosorbent assay in 152 hypertensive and 166 normotensive subjects in whom seven tagging single-nucleotide polymorphisms (SNPs) in the F11R gene had been genotyped.
  
  
  RESULTS
  Plasma sF11R levels were significantly higher in hypertensive subjects than in normotensive subjects (median (interquartile) range): 162.8 (85.5-293.2) vs. 116.5 (74.1-194.8) pg/ml, P = 0.004), which remained significantly higher after adjusting for age, sex, body mass index (BMI), and homeostasis model assessment of insulin resistance (HOMA-IR) (P = 0.028). In stepwise multiple logistic regression, sF11R level (log-transformed) (P = 0.040), triglycerides (log-transformed) (P = 0.024), and HOMA-IR (log-transformed) (P < 0.001) were independently associated with hypertension. Plasma sF11R level correlated with systolic and diastolic blood pressures (r = 0.15, P < 0.001, and r = 0.13, P = 0.024, respectively). In stepwise multiple linear regression, hypertension (P = 0.013) and fibrinogen levels (P = 0.027) were significant independent predictors of sF11R level. A seven-locus haplotype, present in 2.1% of the subjects, was associated with higher sF11R level (P = 0.024).
  
  
  CONCLUSIONS
  These results further support a role of F11 receptor in the pathophysiology of human hypertension.
authors.affiliation: Department of Medicine, University of Hong Kong, Hong Kong, People's Republic of China.
authors.forename: Kwok Leung
authors.initials: KL
authors.lastname: Ong
authors.forename: Raymond Y H
authors.initials: RY
authors.lastname: Leung
authors.forename: Anna
authors.initials: A
authors.lastname: Babinska
authors.forename: Moro O
authors.initials: MO
authors.lastname: Salifu
authors.forename: Yigal H
authors.initials: YH
authors.lastname: Ehrlich
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Kornecki
authors.forename: Louisa Y F
authors.initials: LY
authors.lastname: Wong
authors.forename: Annette W K
authors.initials: AW
authors.lastname: Tso
authors.forename: Stacey S
authors.initials: SS
authors.lastname: Cherny
authors.forename: Pak Chung
authors.initials: PC
authors.lastname: Sham
authors.forename: Tai Hing
authors.initials: TH
authors.lastname: Lam
authors.forename: Karen S L
authors.initials: KS
authors.lastname: Lam
authors.forename: Bernard M Y
authors.initials: BM
authors.lastname: Cheung
mesh_terms: D000368:Aged; D001794:Blood Pressure / Q000235:genetics; D015815:Cell Adhesion Molecules / Q000097:blood*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000235:genetics*; D007333:Insulin Resistance / Q000235:genetics; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D011956:Receptors, Cell Surface / Q000097:blood*; D012044:Regression Analysis
chemical_list: D015815:Cell Adhesion Molecules; C407243:F11R protein, human; D011956:Receptors, Cell Surface