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J. Biol. Chem., Vol. 275, Issue 23, 17527-17535, June 9, 2000
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From the Serum paraoxonase (PON1), present on high density
lipoprotein, may inhibit low density lipoprotein (LDL) oxidation and
protect against atherosclerosis. We generated combined PON1 knockout
(KO)/apolipoprotein E (apoE) KO and apoE KO control mice to compare
atherogenesis and lipoprotein oxidation. Early lesions were examined in
3-month-old mice fed a chow diet, and advanced lesions were examined in
6-month-old mice fed a high fat diet. In both cases, the PON1 KO/apoE
KO mice exhibited significantly more atherosclerosis (50-71%
increase) than controls. We examined LDL oxidation and clearance
in vivo by injecting human LDL into the mice and following
its turnover. LDL clearance was faster in the double KO mice as
compared with controls. There was a greater rate of accumulation of
oxidized phospholipid epitopes and a greater accumulation of
LDL-immunoglobulin complexes in the double KO mice than in controls.
Furthermore, the amounts of three bioactive oxidized phospholipids were
elevated in the endogenous intermediate density lipoprotein/LDL of
double KO mice as compared with the controls. Finally, the expression of heme oxygenase-1, peroxisome proliferator-activated receptor
Combined Serum Paraoxonase Knockout/Apolipoprotein E Knockout
Mice Exhibit Increased Lipoprotein Oxidation and
Atherosclerosis*
§¶,§,§,
,§,,, and§
Division of Cardiology, Department of
Medicine, the § Department of Microbiology and Molecular
Genetics, the ** Department of Pathology, and the
§§ Psychiatry & Biobehavioral Sciences and the
Neuropsychiatric Institute, UCLA, Los Angeles, California 90095, the Division of Endocrinology and Metabolism, Department of
Medicine, University of California, San Diego,
La Jolla, California 92093, and the La
Jolla Institute for Allergy and Immunology,
San Diego, California 92121
,
and oxidized LDL receptors were elevated in the livers of double KO
mice as compared with the controls. These data demonstrate that PON1
deficiency promotes LDL oxidation and atherogenesis in apoE KO mice.
*
This work was supported by United States Public Health
Services Grants HL30568 (to A. J. L. and J. A. B.) and HL56989 (to J. L. W.), and an American Heart Association Greater Los Angeles Affiliate grant (to D. M. S.).The costs of publication of this article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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S. T. Reddy, D. J. Wadleigh, V. Grijalva, C. Ng, S. Hama, A. Gangopadhyay, D. M. Shih, A. J. Lusis, M. Navab, and A. M. Fogelman Human Paraoxonase-3 Is an HDL-Associated Enzyme With Biological Activity Similar to Paraoxonase-1 Protein but Is Not Regulated by Oxidized Lipids Arterioscler. Thromb. Vasc. Biol., April 1, 2001; 21(4): 542 - 547. [Abstract] [Full Text] [PDF]
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Y. Terasawa, Z. Ladha, S. W. Leonard, J. D. Morrow, D. Newland, D. Sanan, L. Packer, M. G. Traber, and R. V. Farese Jr. Increased atherosclerosis in hyperlipidemic mice deficient in alpha -tocopherol transfer protein and vitamin E PNAS, November 22, 2000; (2000) 240462697. [Abstract] [Full Text]
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Y. Terasawa, Z. Ladha, S. W. Leonard, J. D. Morrow, D. Newland, D. Sanan, L. Packer, M. G. Traber, and R. V. Farese Jr. Increased atherosclerosis in hyperlipidemic mice deficient in alpha -tocopherol transfer protein and vitamin E PNAS, December 5, 2000; 97(25): 13830 - 13834. [Abstract] [Full Text] [PDF]
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