title: Upregulation of angiotensin-converting enzyme during the healing process after injury at the site of percutaneous transluminal coronary angioplasty in humans.
abstract: BACKGROUND
  Balloon injury models in rat have shown enhanced expression of ACE in the developing neointima. However, neointimal lesions in human coronary arteries are complex due to atherosclerosis and different types of wall laceration. This study was designed to investigate whether ACE is present in the neointima of humans, including patients with restenosis after percutaneous transluminal coronary angioplasty (PTCA).
  
  
  RESULTS
  Thirty-seven sites with angioplasty injury, obtained at autopsy, were studied using immunocytochemical techniques. Sites with injury limited to a fibrous plaque and those with injury extending into the media (<2 months after PTCA) showed fibrocellular repair tissue composed mainly of smooth muscle cells that were distinctly positive for ACE. In cellular reactions at the site of injury limited to the atheromatous plaque (<2 months after PTCA), the expression of ACE appeared first in accumulated macrophages; once smooth muscle cells appeared in the repair tissue, they also expressed ACE. At a later stage (3 months after PTCA), the number of cells with ACE expression decreased markedly; from 7 months on, ACE was no longer expressed within the repair tissue. Basically, there were no differences with regard to ACE expression during the healing process after PTCA between segments with and those without angiographic evidence of restenosis.
  
  
  CONCLUSIONS
  These results show that PTCA injury in humans results in upregulation of ACE at sites of active repair and, therefore, ACE could play an important role as one of the mediators of the healing process after PTCA.
authors.affiliation: Department of Geriatric Medicine, Osaka University Medical School, Suita, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ohishi
authors.forename: M
authors.initials: M
authors.lastname: Ueda
authors.forename: H
authors.initials: H
authors.lastname: Rakugi
authors.forename: A
authors.initials: A
authors.lastname: Okamura
authors.forename: T
authors.initials: T
authors.lastname: Naruko
authors.forename: A E
authors.initials: AE
authors.lastname: Becker
authors.forename: K
authors.initials: K
authors.lastname: Hiwada
authors.forename: A
authors.initials: A
authors.lastname: Kamitani
authors.forename: K
authors.initials: K
authors.lastname: Kamide
authors.forename: J
authors.initials: J
authors.lastname: Higaki
authors.forename: T
authors.initials: T
authors.lastname: Ogihara
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D002102:Cadaver; D003327:Coronary Disease / Q000503:physiopathology / Q000628:therapy; D003331:Coronary Vessels / Q000293:injuries* / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D007703:Peptidyl-Dipeptidase A / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D012008:Recurrence; D014945:Wound Healing / Q000502:physiology*
chemical_list: D012333:RNA, Messenger; D007703:Peptidyl-Dipeptidase A