title: Characterization of human late outgrowth endothelial progenitor-derived cells under various flow conditions.
abstract: BACKGROUND
  Endothelial progenitor-derived cells (EPC) are a cell therapy tool in peripheral arterial disease and for re-endothelialization of bypasses and stents.
  
  
  OBJECTIVE
  To assess EPC behavior under flow conditions normally found in vivo.
  
  
  RESULTS
  EPC were isolated from human cord blood, cultured on compliant tubes and exposed in an in vitro flow system mimicking hemodynamic environments normally found in medium and large arteries. EPC exposed for 24 h to unidirectional (0.3 ± 0.1 or 6 ± 3 dynes/cm(2)) shear stress oriented along flow direction, while those exposed to bidirectional shear stress (0.3 ± 3 dynes/cm(2)) or static conditions had random orientation. Under bidirectional flow, tissue factor (TF) activity and mRNA expression were significantly increased (2.5- and 7.0-fold) compared to static conditions. Under low shear unidirectional flow TF mRNA increased 4.9 ± 0.5-fold. Similar flow-induced increases were observed for TF in mature umbilical vein-derived endothelial cells. Expression of tissue-type plasminogen activator (t-PA), urokinase (u-PA) and monocyte chemotactic protein 1 (MCP1) were reduced by 40-60% in late outgrowth endothelial progenitor-derived cells (LO-EPC) exposed to any flow environment, while MCP1, but not t-PA or u-PA, was decreased in HUVEC.
  
  
  CONCLUSIONS
  Flow, in particular bidirectional, modifies the hemostatic balance in LO-EPC with increased TF and decreased plasminogen activator expression.
authors.affiliation: Division of Vascular Medicine, University Hospital of Lausanne, Fribourg, Switzerland. lucia.mazzolai@chuv.ch
authors.forename: Lucia
authors.initials: L
authors.lastname: Mazzolai
authors.forename: Karima
authors.initials: K
authors.lastname: Bouzourene
authors.forename: Daniel
authors.initials: D
authors.lastname: Hayoz
authors.forename: Françoise
authors.initials: F
authors.lastname: Dignat-George
authors.forename: Jia Wei
authors.initials: JW
authors.lastname: Liu
authors.forename: Henri
authors.initials: H
authors.lastname: Bounameaux
authors.forename: Sylvie
authors.initials: S
authors.lastname: Dunoyer-Geindre
authors.forename: Egbert K O
authors.initials: EK
authors.lastname: Kruithof
mesh_terms: D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D042783:Endothelial Cells / Q000166:cytology* / Q000502:physiology*; D005312:Fetal Blood / Q000166:cytology; D015870:Gene Expression / Q000502:physiology; D006412:Hematopoietic Stem Cells / Q000166:cytology*; D006801:Humans; D018919:Neovascularization, Physiologic / Q000502:physiology*; D011673:Pulsatile Flow / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism; D013314:Stress, Mechanical; D013925:Thromboplastin / Q000235:genetics / Q000378:metabolism; D010959:Tissue Plasminogen Activator / Q000235:genetics / Q000378:metabolism; D014470:Umbilical Cord / Q000166:cytology; D014568:Urokinase-Type Plasminogen Activator / Q000235:genetics / Q000378:metabolism
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D012333:RNA, Messenger; D013925:Thromboplastin; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator