title: Phenotypic modification of arterial smooth muscle cells in response to medial dissection.
abstract: BACKGROUND
  In the treatment of peripheral arteries, percutaneous transluminal angioplasty is commonly associated with intimal tears and dissections.
  
  
  OBJECTIVE
  To investigate the influence of medial dissection on the remodelling of the vessel wall after balloon injury.
  
  
  METHODS
  Aortae were obtained from 14 Fauve de Bourgogne rabbits that had been fed a normal diet. Seven days after the initial pull-back injury, the aortae were examined using morphometric and immunocytochemical methods.
  
  
  RESULTS
  Eight rabbits (57%) had a tear that extended into the media. Morphometric measurements showed that the intima was significantly thinner when there was a medial dissection [(18.3 +/- 6.9) x 10(-3) versus (39.1 +/- 3.5) x 10(-3) mm without dissection, P < 0.001]. In the media of injured vessels, medial dissection was associated with a greater accumulation of extracellular matrix proteins (50.5 +/- 9.7 versus 12.4 +/- 2.2% of the surface area), a marked reduction in alpha-smooth muscle actin content (36.6 +/- 5.4 versus 47.4 +/- 7.5% of the surface area), a higher expression of a smooth muscle activation antigen (21.2 +/- 5.7 versus 8.9 +/- 1.5% of the 2P1A2-immunostained surface area) and an increase in the number of medial proliferating cell nuclear antigen-positive nuclei (8.2 versus 1.2% of labelled nuclei).
  
  
  CONCLUSIONS
  These observations indicated that mechanical injury of the arterial wall induces a phenotypic activation of medial smooth muscle cells. In the case of acute distension, the response of the smooth muscle cells in the media was mainly responsible for wound healing in the presence of medial dissection; moreover, acute distension induced a significant higher state of activation and a medial repairing that could prevent migration towards the intimal space.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale, Pessac, France.
authors.forename: P
authors.initials: P
authors.lastname: Dufourcq
authors.forename: H
authors.initials: H
authors.lastname: Louis
authors.forename: F
authors.initials: F
authors.lastname: Dandré
authors.forename: J
authors.initials: J
authors.lastname: Lavie
authors.forename: J
authors.initials: J
authors.lastname: Bonnet
authors.forename: J M
authors.initials: JM
authors.lastname: Lamazière
mesh_terms: D000199:Actins / Q000378:metabolism; D000800:Angioplasty, Balloon / Q000009:adverse effects*; D000818:Animals; D001012:Aorta, Abdominal / Q000293:injuries* / Q000378:metabolism; D015415:Biomarkers; D002455:Cell Division; D002465:Cell Movement; D004195:Disease Models, Animal; D004210:Dissection; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D007150:Immunohistochemistry; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000293:injuries / Q000378:metabolism*; D010641:Phenotype; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011817:Rabbits
chemical_list: D000199:Actins; D015415:Biomarkers; D016326:Extracellular Matrix Proteins; D018809:Proliferating Cell Nuclear Antigen