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

Jinyu Wang, Xunde Xian, Wei Huang, Li Chen, Liling Wu, Yi Zhu, Jianglin Fan, Colin Ross, Michael R. Hayden, George Liu

Research output: Contribution to journalArticle

18 Scopus citations

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. METHODS AND 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.

Original languageEnglish (US)
Pages (from-to)197-203
Number of pages7
JournalArteriosclerosis, thrombosis, and vascular biology
Volume27
Issue number1
DOIs
StatePublished - Jan 1 2007

Keywords

  • Atherosclerosis
  • Gene transfer
  • Lipoprotein lipase
  • Mice
  • Vascular cell adhesion molecule-1

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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