title: Transfusion of autologous late-outgrowth endothelial cells reduces arterial neointima formation after injury.
abstract: OBJECTIVE
  Late-outgrowth endothelial cells (OECs) exist in blood and other organs. We aimed to explore whether and how OECs participate in re-endothelialization and prevent vascular neointima formation after injury.
  
  
  RESULTS
  Rabbit bone marrow OECs were cultured for 4 weeks to increase their numbers. Transfusion of autologous OECs (2 × 10⁶-1 × 10⁷/kg) soon after rabbit ear central artery injury reduced the increase in intima area and the decrease in lumen area observed at days 14 and 28. Transfusion of autologous OECs (1 × 10⁷/kg) ameliorated some early (days 2 and 7) inflammatory and angiogenic responses (local and systemic) to the injury. Red fluorescence was seen within 7 days after transfusion of 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine-labelled acetylated low-density lipoprotein (Dil-acLDL)-incorporated OECs, and 1 h after perfusion of the isolated rabbit ear with Ringer-Locke solution containing Dil-acLDL-incorporated OECs, in the injured rabbit ear central artery. After transfusion of 5-bromo-2'-deoxyuridine (BrdU) incorporated autologous OECs, BrdU-positive cells appeared in the injured artery intima at day 3 and were present in the rescued artery endothelium at day 28. The OECs, ranging from 5%-15% of vascular smooth muscle cells (VSMCs), and the OEC-conditioned medium (5-15%) both inhibited VSMC proliferation and migration in vitro and regulated the arrangement of VSMCs. The VSMCs were helpful for OECs to form tubes in vitro.
  
  
  CONCLUSIONS
  Circulating OECs participate in re-endothelialization directly and inhibit VSMC migration and proliferation by a paracrine pathway; transfusion of large numbers of autologous OECs soon after vascular injury may prevent neointima formation.
authors.affiliation: Department of Pharmacology, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi, 710061, China.
authors.forename: Shu-Qin
authors.initials: SQ
authors.lastname: Liu
authors.forename: Zeng-Li
authors.initials: ZL
authors.lastname: Li
authors.forename: Yong-Xiao
authors.initials: YX
authors.lastname: Cao
authors.forename: Le
authors.initials: L
authors.lastname: Li
authors.forename: Xin
authors.initials: X
authors.lastname: Ma
authors.forename: Xiao-Ge
authors.initials: XG
authors.lastname: Zhao
authors.forename: Ai-Qun
authors.initials: AQ
authors.lastname: Kang
authors.forename: Chuan-Hao
authors.initials: CH
authors.lastname: Liu
authors.forename: Bing-Xiang
authors.initials: BX
authors.lastname: Yuan
mesh_terms: D042501:Angiogenic Proteins / Q000097:blood; D000818:Animals; D001158:Arteries / Q000293:injuries / Q000473:pathology / Q000601:surgery; D002448:Cell Adhesion; D002465:Cell Movement; D049109:Cell Proliferation; D002478:Cells, Cultured; D017077:Culture Media, Conditioned / Q000378:metabolism; D004195:Disease Models, Animal; D004423:Ear / Q000098:blood supply*; D042783:Endothelial Cells / Q000378:metabolism / Q000637:transplantation*; D006965:Hyperplasia; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000293:injuries / Q000473:pathology / Q000601:surgery; D019899:Paracrine Communication; D011817:Rabbits; D013997:Time Factors; D014182:Transplantation, Autologous; D017539:Tunica Intima / Q000293:injuries / Q000473:pathology / Q000601:surgery*; D057772:Vascular System Injuries / Q000097:blood / Q000473:pathology / Q000601:surgery*
chemical_list: D042501:Angiogenic Proteins; D017077:Culture Media, Conditioned; D018836:Inflammation Mediators