title: Arterial wall response to ex vivo exposure to oscillatory shear stress.
abstract: BACKGROUND
  The aim of this study was to analyze the arterial wall response to plaque-prone hemodynamic environments, known to occur mainly in areas of arterial trees such as bifurcations and branching points. In these areas, the vasculature is exposed to cyclically reversing flow that induces an endothelial dysfunction predisposing thus arteries to local development of atherosclerotic plaques.
  
  
  METHODS
  We used an ex vivo perfusion system that allows culturing arterial segments under different hemodynamic conditions. Porcine carotid arteries were exposed for 3 days to unidirectional high and low shear stress (6 +/- 3 and 0.3 +/- 0.1 dyn/cm(2)) as well as to oscillatory shear stress (0.3 +/- 3 dyn/cm(2)). This latter condition mimics the hemodynamics present at plaque-prone areas. At the end of the perfusion, the influence of different flow patterns on arterial metabolism was assessed in terms of matrix turnover as well as of smooth muscle cell function, differentiation and migration.
  
  
  RESULTS
  Our results show that after 3 days of perfusion none of the applied conditions influence smooth muscle cell phenotype retaining their full contraction capacity. However, an increase in the expression level of matrix metalloproteinase-2 and -9, as well as a decrease in plasminogen activator inhibitor-1 expression were observed in arteries exposed to oscillatory shear stress when compared to arteries exposed to unidirectional shear stress.
  
  
  CONCLUSIONS
  These observations suggest that plaque-prone hemodynamic environment triggers a vascular wall remodelling process and promotes changes in arterial wall metabolism, with important implication in atherogenesis.
authors.affiliation: Laboratory of Hemodynamics and Cardiovascular Technology, Swiss Federal Institute of Technology, Lausanne, Switzerland. veronica.gambillara@epfl.ch
authors.forename: Veronica
authors.initials: V
authors.lastname: Gambillara
authors.forename: Gabriela
authors.initials: G
authors.lastname: Montorzi
authors.forename: Christelle
authors.initials: C
authors.lastname: Haziza-Pigeon
authors.forename: Nikos
authors.initials: N
authors.lastname: Stergiopulos
authors.forename: Paolo
authors.initials: P
authors.lastname: Silacci
mesh_terms: D000818:Animals; D002339:Carotid Arteries / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D049109:Cell Proliferation; D066298:In Vitro Techniques; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology; D032389:Myocytes, Smooth Muscle / Q000166:cytology / Q000502:physiology; D010641:Phenotype; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D013314:Stress, Mechanical; D013552:Swine; D014018:Tissue Distribution; D014661:Vasoconstriction
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9