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Journal of Lipid Research, Vol. 41, 1495-1508, September 2000
Copyright © 2000 by Lipid Research, Inc.
Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: steps 2 and 3
Mohamad Navaba,
Susan Y. Hamaa,
G. M. Anantharamaiahb,
Kholood Hassana,
Greg P. Hougha,
Andrew D. Watsona,
Srinivasa T. Reddya,
Alex Sevanianc,
Gregg C. Fonarowa, and
Alan M. Fogelmana
a Atherosclerosis Research Unit, Division of Cardiology, Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095
b Department of Medicine and the Atherosclerosis Research Unit, University of Alabama, Birmingham, AL 35294
c Psychiatry and Biobehavioral Sciences, Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, Los Angeles, CA 90089
Correspondence to:
Alan M. Fogelman
Treatment of human artery wall cells with apolipoprotein A-I (apoA-I), but not apoA-II, with an apoA-I peptide mimetic, or with high density lipoprotein (HDL), or paraoxonase, rendered the cells unable to oxidize low density lipoprotein (LDL). Human aortic wall cells were found to contain 12-lipoxygenase (12-LO) protein. Transfection of the cells with antisense to 12-LO (but not sense) eliminated the 12-LO protein and prevented LDL-induced monocyte chemotactic activity. Addition of 13(S)-hydroperoxyoctadecadienoic acid [13(S)-HPODE] and 15(S)-hydroperoxyeicosatetraenoic acid [15(S)-HPETE] dramatically enhanced the nonenzymatic oxidation of both 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (PAPC) and cholesteryl linoleate. On a molar basis 13(S)-HPODE and 15(S)-HPETE were approximately two orders of magnitude greater in potency than hydrogen peroxide in causing the formation of biologically active oxidized phospholipids (m/z 594, 610, and 828) from PAPC. Purified paraoxonase inhibited the biologic activity of these oxidized phospholipids. HDL from 10 of 10 normolipidemic patients with coronary artery disease, who were neither diabetic nor receiving hypolipidemic medications, failed to inhibit LDL oxidation by artery wall cells and failed to inhibit the biologic activity of oxidized PAPC, whereas HDL from 10 of 10 age- and sex-matched control subjects did.
We conclude that a) mildly oxidized LDL is formed in three steps, one of which involves 12-LO and each of which can be inhibited by normal HDL, and b) HDL from at least some coronary artery disease patients with normal blood lipid levels is defective both in its ability to prevent LDL oxidation by artery wall cells and in its ability to inhibit the biologic activity of oxidized PAPC.Navab, M., S. Y. Hama, G. M. Anantharamaiah, K. Hassan, G. P. Hough, A. D. Watson, S. T. Reddy, A. Sevanian, G. C. Fonarow, and A. M. Fogelman. Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: steps 2 and 3. J. Lipid Res. 2000. 41: 1495;1508.
Supplementary key words:
LDL, HDL, mildly oxidized LDL, MM-LDL, oxidized phospholipids, HPODE, HPETE, cholesteryl linoleate hydroperoxide, paraoxonase, atherosclerosis, antioxidant

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P. Holvoet, K. Peeters, S. Lund-Katz, A. Mertens, P. Verhamme, R. Quarck, D. Stengel, M. Lox, E. Deridder, H. Bernar, et al.
Arg123-Tyr166 Domain of Human ApoA-I Is Critical for HDL-Mediated Inhibition of Macrophage Homing and Early Atherosclerosis in Mice
Arterioscler. Thromb. Vasc. Biol.,
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M. Navab, B. J. Van Lenten, S. T. Reddy, and A. M. Fogelman
High-Density Lipoprotein and the Dynamics of Atherosclerotic Lesions
Circulation,
November 13, 2001;
104(20):
2386 - 2387.
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P. K. Shah, S. Kaul, J. Nilsson, and B. Cercek
Exploiting the Vascular Protective Effects of High-Density Lipoprotein and Its Apolipoproteins: An Idea Whose Time for Testing Is Coming, Part I
Circulation,
November 6, 2001;
104(19):
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C.-y. Yang, J. Wang, A. N. Krutchinsky, B. T. Chait, J. D. Morrisett, and C. V. Smith
Selective oxidation in vitro by myeloperoxidase of the N-terminal amine in apolipoprotein B-100
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November 1, 2001;
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[Abstract]
[Full Text]
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A. MERTENS and P. HOLVOET
Oxidized LDL and HDL: antagonists in atherothrombosis
FASEB J,
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[Abstract]
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B. C. Y. Wong, W. P. Wang, C. H. Cho, X. M. Fan, M. C. M. Lin, H. F. Kung, and S. K. Lam
12-Lipoxygenase inhibition induced apoptosis in human gastric cancer cells
Carcinogenesis,
September 1, 2001;
22(9):
1349 - 1354.
[Abstract]
[Full Text]
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R. Natarajan, M. A. Reddy, K. U. Malik, S. Fatima, and B. V. Khan
Signaling Mechanisms of Nuclear Factor-{kappa}B-Mediated Activation of Inflammatory Genes by 13-Hydroperoxyoctadecadienoic Acid in Cultured Vascular Smooth Muscle Cells
Arterioscler. Thromb. Vasc. Biol.,
September 1, 2001;
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[Abstract]
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B. Mackness, G. K. Davies, W. Turkie, E. Lee, D. H. Roberts, E. Hill, C. Roberts, P. N. Durrington, and M. I. Mackness
Paraoxonase Status in Coronary Heart Disease: Are Activity and Concentration More Important Than Genotype?
Arterioscler. Thromb. Vasc. Biol.,
September 1, 2001;
21(9):
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[Abstract]
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M. Navab, S. Y. Hama, G. P. Hough, G. Subbanagounder, S. T. Reddy, and A. M. Fogelman
A cell-free assay for detecting HDL that is dysfunctional in preventing the formation of or inactivating oxidized phospholipids
J. Lipid Res.,
August 1, 2001;
42(8):
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[Abstract]
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G. Datta, M. Chaddha, S. Hama, M. Navab, A. M. Fogelman, D. W. Garber, V. K. Mishra, R. M. Epand, R. F. Epand, S. Lund-Katz, et al.
Effects of increasing hydrophobicity on the physical-chemical and biological properties of a class A amphipathic helical peptide
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July 1, 2001;
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[Abstract]
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B. J. Van Lenten, A. C. Wagner, D. P. Nayak, S. Hama, M. Navab, and A. M. Fogelman
High-Density Lipoprotein Loses Its Anti-Inflammatory Properties During Acute Influenza A Infection
Circulation,
May 8, 2001;
103(18):
2283 - 2288.
[Abstract]
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D. W. Garber, G. Datta, M. Chaddha, M. N. Palgunachari, S. Y. Hama, M. Navab, A. M. Fogelman, J. P. Segrest, and G. M. Anantharamaiah
A new synthetic class A amphipathic peptide analogue protects mice from diet-induced atherosclerosis
J. Lipid Res.,
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[Abstract]
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M. Navab, J. A. Berliner, G. Subbanagounder, S. Hama, A. J. Lusis, L. W. Castellani, S. Reddy, D. Shih, W. Shi, A. D. Watson, et al.
HDL and the Inflammatory Response Induced by LDL-Derived Oxidized Phospholipids
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April 1, 2001;
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481 - 488.
[Abstract]
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M. Navab, S. Y. Hama, C. J. Cooke, G. M. Anantharamaiah, M. Chaddha, L. Jin, G. Subbanagounder, K. F. Faull, S. T. Reddy, N. E. Miller, et al.
Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: step 1
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C. C. Curtain, F. Ali, I. Volitakis, R. A. Cherny, R. S. Norton, K. Beyreuther, C. J. Barrow, C. L. Masters, A. I. Bush, and K. J. Barnham
Alzheimer's Disease Amyloid-beta Binds Copper and Zinc to Generate an Allosterically Ordered Membrane-penetrating Structure Containing Superoxide Dismutase-like Subunits
J. Biol. Chem.,
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[Abstract]
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C. J. Ng, D. J. Wadleigh, A. Gangopadhyay, S. Hama, V. R. Grijalva, M. Navab, A. M. Fogelman, and S. T. Reddy
Paraoxonase-2 Is a Ubiquitously Expressed Protein with Antioxidant Properties and Is Capable of Preventing Cell-mediated Oxidative Modification of Low Density Lipoprotein
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[Abstract]
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Copyright © 2000 by the American Society for Biochemistry and Molecular Biology.
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