title: Association of plasma levels of F11 receptor/junctional adhesion molecule-A (F11R/JAM-A) with human atherosclerosis.
abstract: OBJECTIVE
  The purpose of this study was to determine the association of the F11 receptor (F11R) with human vascular disease.
  
  
  BACKGROUND
  A molecule identified as critical for platelet adhesion to a cytokine-inflamed endothelial surface in vitro is F11R. The F11R is known to be expressed in platelets and endothelium and reported recently to be overexpressed in atherosclerotic plaques.
  
  
  METHODS
  A novel enzyme-linked immunosorbent assay was developed for the measurement of soluble F11R in human plasma. The F11R levels, along with a number of other biomarkers, were measured in 389 male patients with known or suspected coronary artery disease (CAD) undergoing coronary angiography at a Veterans Administration Medical Center.
  
  
  RESULTS
  Patients with normal or nonobstructive disease (CAD angiographic score of 0), mild-to-moderate disease (score of 1 to 3), and severe disease (score of 4 to 6) had median F11R plasma levels of 38.6 pg/ml (mean 260 +/- 509.6 pg/ml), 45.2 pg/ml (mean 395.3 +/- 752.7 pg/ml), and 105.8 pg/ml (mean 629 +/- 831.7 pg/ml), respectively (p = 0.03). By multivariate analysis, the variables independently associated with CAD score were age, hyperlipidemia, chronic renal insufficiency, left ventricular function, and plasma F11R levels. The F11R was the only biomarker that was independently associated with CAD score. Consistent with the previously reported effects of tumor necrosis factor (TNF)-alpha on F11R expression in cultured endothelial cells, F11R levels correlated strongly with plasma TNF-alpha levels (r = 0.84; p < 0.0001).
  
  
  CONCLUSIONS
  Plasma F11R is independently associated with the presence and severity of angiographically defined CAD. By virtue of its strong correlation to plasma TNF-alpha, F11R may be an important mediator of the effects of inflammation on the vessel wall. Strategies that block F11R may represent a novel approach to the treatment of human atherosclerosis.
authors.affiliation: Division of Cardiology, Department of Medicine, State University of New York Downstate Medical Center, Brooklyn, New York 11203-2098, USA. ecavusoglu@aol.com
authors.forename: Erdal
authors.initials: E
authors.lastname: Cavusoglu
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Kornecki
authors.forename: Malgorzata B
authors.initials: MB
authors.lastname: Sobocka
authors.forename: Anna
authors.initials: A
authors.lastname: Babinska
authors.forename: Yigal H
authors.initials: YH
authors.lastname: Ehrlich
authors.forename: Vineet
authors.initials: V
authors.lastname: Chopra
authors.forename: Sunitha
authors.initials: S
authors.lastname: Yanamadala
authors.forename: Cyril
authors.initials: C
authors.lastname: Ruwende
authors.forename: Moro O
authors.initials: MO
authors.lastname: Salifu
authors.forename: Luther T
authors.initials: LT
authors.lastname: Clark
authors.forename: Calvin
authors.initials: C
authors.lastname: Eng
authors.forename: David J
authors.initials: DJ
authors.lastname: Pinsky
authors.forename: Jonathan D
authors.initials: JD
authors.lastname: Marmur
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000097:blood*; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood* / Q000000981:diagnostic imaging / Q000209:etiology; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D007136:Immunoglobulins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011956:Receptors, Cell Surface / Q000097:blood*; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; D015815:Cell Adhesion Molecules; C407243:F11R protein, human; D007136:Immunoglobulins; D011956:Receptors, Cell Surface; D014409:Tumor Necrosis Factor-alpha