title: E-selectin blockade decreases adventitial inflammation and attenuates intimal hyperplasia in rat carotid arteries after balloon injury.
abstract: OBJECTIVE
  Inflammation is one of the initial repair processes after vascular injury. E-selectin facilitates adherence of leukocytes to vascular endothelium at the site of inflammation. Because the role of E-selectin in this process is not fully understood, we studied the role of E-selectin in vascular injury with a flow chamber model and a rat model of carotid artery injury.
  
  
  RESULTS
  We established a rat aortic endothelial cell (RAEC) culture system from the aortas of adult male rats. When rat myelomonocytes were suspended in a flow chamber, rolling and adhesion to lipopolysaccharide (LPS)-stimulated RAECs were observed. Cell rolling and adhesion were greatly reduced by addition of anti-E-selectin monoclonal antibody (mAb). We then induced balloon injury in the left carotid arteries of rats. E-selectin expression was enhanced in endothelial cells at adventitial small vessels 7 days after injury. Rats with balloon injury were injected intraperitoneally with anti-E-selectin mAb for 8 days. Inflammatory cell infiltration was reduced by anti-E-selectin mAb treatment at the adventitia at 7 days after injury. This reduction was associated with attenuation of intimal hyperplasia in the rats treated with the mAb.
  
  
  CONCLUSIONS
  These data suggest that E-selectin regulates adventitial inflammation through leukocyte adhesion and contributes to the process of intimal hyperplasia after balloon injury.
authors.affiliation: Department of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Ryo
authors.initials: R
authors.lastname: Gotoh
authors.forename: Jun-ichi
authors.initials: J
authors.lastname: Suzuki
authors.forename: Hisanori
authors.initials: H
authors.lastname: Kosuge
authors.forename: Tsunekazu
authors.initials: T
authors.lastname: Kakuta
authors.forename: Shinji
authors.initials: S
authors.lastname: Sakamoto
authors.forename: Masayuki
authors.initials: M
authors.lastname: Yoshida
authors.forename: Mitsuaki
authors.initials: M
authors.lastname: Isobe
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D019138:Antibodies, Blocking / Q000494:pharmacology*; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D001011:Aorta / Q000737:chemistry / Q000166:cytology / Q000378:metabolism; D016466:CHO Cells / Q000737:chemistry / Q000378:metabolism; D002339:Carotid Arteries / Q000737:chemistry / Q000166:cytology / Q000378:metabolism; D020212:Carotid Artery Injuries / Q000150:complications*; D002460:Cell Line; D045744:Cell Line, Tumor; D003238:Connective Tissue / Q000098:blood supply / Q000276:immunology / Q000473:pathology; D006224:Cricetinae; D003412:Cricetulus / Q000235:genetics; D004195:Disease Models, Animal; D019040:E-Selectin / Q000096:biosynthesis / Q000276:immunology* / Q000502:physiology; D042783:Endothelial Cells / Q000737:chemistry / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology / Q000254:growth & development / Q000276:immunology; D018922:HL-60 Cells / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006965:Hyperplasia / Q000517:prevention & control*; D066298:In Vitro Techniques; D007249:Inflammation / Q000517:prevention & control; D007962:Leukocytes / Q000276:immunology / Q000378:metabolism; D008297:Male; D009389:Neovascularization, Pathologic / Q000517:prevention & control; D051381:Rats; D017207:Rats, Sprague-Dawley; D017539:Tunica Intima / Q000254:growth & development / Q000276:immunology / Q000473:pathology
chemical_list: D000893:Anti-Inflammatory Agents; D019138:Antibodies, Blocking; D000911:Antibodies, Monoclonal; D019040:E-Selectin