title: Inhibition of intimal hyperplasia after balloon injury by antibodies to intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1.
abstract: BACKGROUND
  Although intercellular adhesion molecule-1 (ICAM-1) is known to be expressed in balloon-injured arteries, it remains unknown whether ICAM-1 plays a role in the progression of intimal hyperplasia (IH) induced by balloon injury.
  
  
  RESULTS
  We examined the ICAM-1 expression in rat carotid arteries at 1, 2, 5, 7, 10, and 14 days after injury by immunohistochemistry. Medial smooth muscle cells (SMC) expressed ICAM-1 intensely at 1 to 2 days after injury. The regenerating endothelial cells expressed ICAM-1 more than did those of intact carotid arteries. To investigate the effects of monoclonal antibodies (MAbs) on IH, we examined the intima/ medial ratio of arteries at 2 weeks after injury in five treatment groups: nonimmune IgG, anti-membrane glycoprotein MAb, anti-lymphocyte function-associated antigen-1 (LFA-1) MAb, anti-ICAM-1 MAb, and anti-ICAM/LFA-1 MAb. Treatments were administered intravenously into rats for 6 consecutive days after injury. MAb against LFA-1 alone or membrane glycoprotein had no effect on IH. The intima/media ratios in anti-ICAM-1 MAb-treated and anti-ICAM-1/LFA-1 MAb-treated animals were significantly less than those in nonimmune IgG-treated and anti-membrane glycoprotein MAb-treated animals (P < .05).
  
  
  CONCLUSIONS
  Balloon injury induced or upregulated the ICAM-1 expression on vascular SMC and on regenerating endothelial cells. MAb against ICAM-1 or ICAM-1/LFA-1 attenuated IH. These results suggest that ICAM-1 may play a role in the progression of IH after injury in rats.
authors.affiliation: Department of Pathology II, Kurume University School of Medicine, Fukuoka, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Yasukawa
authors.forename: T
authors.initials: T
authors.lastname: Imaizumi
authors.forename: H
authors.initials: H
authors.lastname: Matsuoka
authors.forename: A
authors.initials: A
authors.lastname: Nakashima
authors.forename: M
authors.initials: M
authors.lastname: Morimatsu
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D002339:Carotid Arteries / Q000276:immunology; D002404:Catheterization; D006965:Hyperplasia; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology* / Q000378:metabolism; D016169:Lymphocyte Function-Associated Antigen-1 / Q000276:immunology*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D017539:Tunica Intima / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*
chemical_list: D000911:Antibodies, Monoclonal; D016169:Lymphocyte Function-Associated Antigen-1; D018799:Intercellular Adhesion Molecule-1