title: Expression of LPL in endothelial-intact artery results in lipid deposition and vascular cell adhesion molecule-1 upregulation in both LPL and ApoE-deficient mice.
abstract: OBJECTIVE
  Overexpression of lipoprotein lipase (LPL) in deendothelialized artery led to profound localized lipid deposition. In this study the role of LPL in atherogenesis in endothelial-intact carotid arteries was assessed in genetically hyperlipidemic LPL- and ApoE-deficient mice.
  
  
  RESULTS
  Human wild-type LPL (hLPLwt), catalytically inactive LPL (hLPL194), or control alkaline phosphatase (hAP) were expressed in endothelial-intact carotid arteries via adenoviral vectors. Compared with Ad-hAP, lipid deposition in the arterial wall increased 10.0- and 5.1-fold for Ad-hLPLwt and Ad-hLPL194 in LPL-deficient mice, and 10.6- and 6.2-fold in ApoE-deficient mice, respectively. Vascular cell adhesion molecule-1 (VCAM-1) was upregulated in Ad-hLPLwt and Ad-hLPL194 transferred arteries.
  
  
  CONCLUSIONS
  Endothelial cell associated LPL, either active or inactive, in the arterial wall is a strong proatherosclerotic factor in both LPL- and ApoE-deficient mice.
authors.affiliation: Institute of Cardiovascular Sciences, Peking University Health Science Center, 38 Xueyuan Road, Hai Dian District, 100083, Beijing, China.
authors.forename: Jinyu
authors.initials: J
authors.lastname: Wang
authors.forename: Xunde
authors.initials: X
authors.lastname: Xian
authors.forename: Wei
authors.initials: W
authors.lastname: Huang
authors.forename: Li
authors.initials: L
authors.lastname: Chen
authors.forename: Liling
authors.initials: L
authors.lastname: Wu
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhu
authors.forename: Jianglin
authors.initials: J
authors.lastname: Fan
authors.forename: Colin
authors.initials: C
authors.lastname: Ross
authors.forename: Michael R
authors.initials: MR
authors.lastname: Hayden
authors.forename: George
authors.initials: G
authors.lastname: Liu
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics / Q000378:metabolism*; D002339:Carotid Arteries / Q000378:metabolism* / Q000473:pathology; D002448:Cell Adhesion / Q000235:genetics / Q000502:physiology; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation / Q000235:genetics / Q000502:physiology; D006801:Humans; D006937:Hypercholesterolemia / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D015228:Hypertriglyceridemia / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D050356:Lipid Metabolism / Q000235:genetics / Q000502:physiology*; D008071:Lipoprotein Lipase / Q000235:genetics / Q000378:metabolism*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009000:Monocytes / Q000166:cytology; D015854:Up-Regulation / Q000235:genetics / Q000502:physiology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism*
chemical_list: D001057:Apolipoproteins E; D019010:Vascular Cell Adhesion Molecule-1; D008071:Lipoprotein Lipase