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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apolipoproteins E / genetics
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Apolipoproteins E / metabolism*
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Carotid Arteries / metabolism*
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Carotid Arteries / pathology
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Cell Adhesion / genetics
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Cell Adhesion / physiology
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Cells, Cultured
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Endothelium, Vascular / metabolism*
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Endothelium, Vascular / pathology
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Female
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Gene Expression Regulation / genetics
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Gene Expression Regulation / physiology
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Humans
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Hypercholesterolemia / genetics
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Hypercholesterolemia / metabolism
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Hypercholesterolemia / pathology
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Hypertriglyceridemia / genetics
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Hypertriglyceridemia / metabolism
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Hypertriglyceridemia / pathology
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Lipid Metabolism / genetics
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Lipid Metabolism / physiology*
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Lipoprotein Lipase / genetics
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Lipoprotein Lipase / metabolism*
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Male
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Mice
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Mice, Knockout
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Monocytes / cytology
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Up-Regulation / genetics
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Up-Regulation / physiology*
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Vascular Cell Adhesion Molecule-1 / genetics
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Vascular Cell Adhesion Molecule-1 / metabolism*
Substances
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Apolipoproteins E
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Vascular Cell Adhesion Molecule-1
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Lipoprotein Lipase