title: Modulation of circulating cellular adhesion molecules in postmenopausal women with coronary artery disease.
abstract: OBJECTIVE
  The present study examined the association of estrogen (E2) and the inflammatory response of endothelium in coronary artery disease (CAD) by measuring circulating cellular adhesion molecules (cCAMs) in subjects with atherosclerosis.
  
  
  BACKGROUND
  Atherosclerotic plaque demonstrates features similar to inflammation. Endothelial cell activation by inflammatory cytokines induces expression of cellular adhesion molecules (CAMs), thereby perhaps augmenting leukocyte adhesion and recruitment and subsequent development of atherosclerosis. The incidence of CAD is lower in women; this may be due to the cardioprotective effects of E2.
  
  
  METHODS
  Consecutive eligible subjects with CAD admitted for cardiac catheterization were studied. The groups evaluated were men, postmenopausal women receiving E2 replacement therapy (ERT), postmenopausal women not receiving ERT and premenopausal women. Control groups included men and women without CAD. Preprocedural blood samples were drawn from all groups. Measurements of cCAMs, E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 were performed by enzyme-linked immunoabsorbant assay. E2 levels were assessed by radioimmunoassay.
  
  
  RESULTS
  We observed a statistically significant increase in all cCAMs in men with CAD and postmenopausal women with CAD not receiving ERT compared with postmenopausal women with CAD receiving ERT. Premenopausal women with CAD and postmenopausal women with CAD receiving ERT had a significant increase in VCAM-1 alone compared with the female control group.
  
  
  CONCLUSIONS
  A possible mechanism by which E2 exerts one of its cardioprotective effects is by limiting the inflammatory response to injury by modulating the expression of CAMs from the endothelium.
authors.affiliation: Division of Cardiovascular Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8017, USA. teresa.caulin-glaser@yale.edu
authors.forename: T
authors.initials: T
authors.lastname: Caulin-Glaser
authors.forename: W J
authors.initials: WJ
authors.lastname: Farrell
authors.forename: S E
authors.initials: SE
authors.lastname: Pfau
authors.forename: B
authors.initials: B
authors.lastname: Zaret
authors.forename: K
authors.initials: K
authors.lastname: Bunger
authors.forename: J F
authors.initials: JF
authors.lastname: Setaro
authors.forename: J J
authors.initials: JJ
authors.lastname: Brennan
authors.forename: J R
authors.initials: JR
authors.lastname: Bender
authors.forename: M W
authors.initials: MW
authors.lastname: Cleman
authors.forename: H S
authors.initials: HS
authors.lastname: Cabin
authors.forename: M S
authors.initials: MS
authors.lastname: Remetz
mesh_terms: D000328:Adult; D015815:Cell Adhesion Molecules / Q000097:blood*; D003324:Coronary Artery Disease / Q000097:blood* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D015914:Estrogen Replacement Therapy; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D017698:Postmenopause / Q000502:physiology; D011863:Radioimmunoassay
chemical_list: D015815:Cell Adhesion Molecules; D004967:Estrogens