title: A Preliminary Study of the Therapeutic Role of Human Early Fetal Aorta-derived Endothelial Progenitor Cells in Inhibiting Carotid Artery Neointimal Hyperplasia.
abstract: BACKGROUND
  Endothelial cell damage is an important pathophysiological step of restenosis after angioplasty and stenting. Cell transplantation has great therapeutic potential for endothelial recovery. We investigated the effect of transplanting endothelial progenitor cells (EPCs) derived from human early fetal aortas in rat injured arteries.
  
  
  METHODS
  The carotid arterial endothelium of Sprague-Dawley rats was damaged by dilatation with a 1.5 F balloon catheter, and then EPCs derived from human early fetal aortas (<14 weeks) were injected into the lumen of the injured artery in transplanted rats, with an equal volume of normal saline injected into control rats. Rats were sacrificed at 2 and 4 weeks after treatment and transplanted cells were identified by immunohistochemical staining with anti-human CD31 and anti-human mitochondria antibodies. Arterial cross-sections were analyzed by pathology, immunohistochemistry, and morphometry.
  
  
  RESULTS
  Green fluorescence-labeled EPCs could be seen in the endovascular surface of balloon-injured vessels after transplantation. The intimal area and intimal/medial area ratio were significantly smaller in the transplanted group than in the control (P < 0.05) and the residual lumen area was larger (P < 0.05). After EPC transplantation, a complete vascular endothelial layer was formed, which was positive for human von Willebrand factor after immunohistochemical staining, and immunohistochemical staining revealed many CD31- and mitochondria-positive cells in the re-endothelialized endothelium with EPC transplantation but not control treatment.
  
  
  CONCLUSIONS
  EPCs derived from human early fetal aorta were successfully transplanted into injured vessels and might inhibit neointimal hyperplasia after vascular injury.
authors.forename: Rong-Wei
authors.initials: RW
authors.lastname: Xu
authors.forename: Wen-Jian
authors.initials: WJ
authors.lastname: Zhang
authors.forename: Jian-Bin
authors.initials: JB
authors.lastname: Zhang
authors.forename: Jian-Yan
authors.initials: JY
authors.lastname: Wen
authors.forename: Meng
authors.initials: M
authors.lastname: Wang
authors.forename: Hong-Lin
authors.initials: HL
authors.lastname: Liu
authors.forename: Lin
authors.initials: L
authors.lastname: Pan
authors.forename: Chang-An
authors.initials: CA
authors.lastname: Yu
authors.forename: Jin-Ning
authors.initials: JN
authors.lastname: Lou
authors.affiliation: Department of Cardiovascular Surgery, China-Japan Friendship Hospital, Beijing 100029; Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100073, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Liu
mesh_terms: D000818:Animals; D002339:Carotid Arteries / Q000473:pathology*; D002448:Cell Adhesion / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D017690:Cell Transplantation; D066026:Endothelial Progenitor Cells / Q000166:cytology* / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D008856:Microscopy, Fluorescence; D058426:Neointima / Q000628:therapy*; D051381:Rats; D017207:Rats, Sprague-Dawley