title: High-density lipoproteins enhance progenitor-mediated endothelium repair in mice.
abstract: OBJECTIVE
  We quantified endothelial progenitor cell (EPC) engraftment into the endothelial layer as an index of progenitor-mediated endothelial repair. Studies were conducted in C57BL/6J and in apolipoprotein E-deficient (apoE(-/-)) mice. We also investigated the possibility that high-density lipoproteins (HDL) may promote progenitor-mediated endothelial repair.
  
  
  RESULTS
  Thoracic aortic sections from C57BL/6J and apoE(-/-) mice were analyzed for evidence of progenitor-derived endothelium as determined by the number of stem cell antigen-1-positive (Sca-1+) cells in the endothelial layer. EPCs (Sca-1+ cells) were significantly increased after endothelial damage induced by lipopolysaccharide (LPS) administration in C57BL/6J mice. The number of EPCs was greater in the aortic endothelium of untreated apoE(-/-) than in untreated C57BL/6J mice and was similar to the number observed in LPS-treated C57BL/6J mice. The number of EPCs in the aortic endothelium of apoE(-/-) mice more than doubled after intravenous infusion of reconstituted HDL.
  
  
  CONCLUSIONS
  EPCs are recruited into the aortic endothelial layer of mice in response to an inflammatory insult. EPCs are also increased in the aortic endothelium of untreated apoE(-/-) mice. The observation that number is further increased in apoE(-/-) mice after injection of HDL suggests a role for HDL in promoting progenitor-mediated endothelial repair.
authors.affiliation: Heart Research Institute, Sydney, NSW 2050, Australia.
authors.forename: Colin
authors.initials: C
authors.lastname: Tso
authors.forename: Gary
authors.initials: G
authors.lastname: Martinic
authors.forename: Wen-Hua
authors.initials: WH
authors.lastname: Fan
authors.forename: Campbell
authors.initials: C
authors.lastname: Rogers
authors.forename: Kerry-Anne
authors.initials: KA
authors.lastname: Rye
authors.forename: Philip J
authors.initials: PJ
authors.lastname: Barter
mesh_terms: D000818:Animals; D000950:Antigens, Ly / Q000032:analysis; D001057:Apolipoproteins E / Q000172:deficiency / Q000502:physiology; D017209:Apoptosis; D050197:Atherosclerosis / Q000517:prevention & control; D042783:Endothelial Cells / Q000737:chemistry / Q000187:drug effects / Q000502:physiology*; D006412:Hematopoietic Stem Cells / Q000502:physiology*; D017493:Leukocyte Common Antigens / Q000032:analysis; D008070:Lipopolysaccharides / Q000633:toxicity; D008075:Lipoproteins, HDL / Q000494:pharmacology*; D008297:Male; D008565:Membrane Proteins / Q000032:analysis; D051379:Mice; D008810:Mice, Inbred C57BL; D011994:Recombinant Proteins / Q000494:pharmacology
chemical_list: D000950:Antigens, Ly; D001057:Apolipoproteins E; D008070:Lipopolysaccharides; D008075:Lipoproteins, HDL; C074650:Ly6a protein, mouse; D008565:Membrane Proteins; D011994:Recombinant Proteins; D017493:Leukocyte Common Antigens