Phospholipid Transfer Protein Deficiency Protects Circulating Lipoproteins from Oxidation Due to the Enhanced Accumulation of Vitamin E
| Autor: | Florent Lalanne, Valéerie Deckert, Joseph L. Witztum, Catherine Desrumaux, Martina Schneider, Anne Athias, Xian-Cheng Jiang, Shucun Qin, Laurent Lagrost, Min Lin, Alan R. Tall |
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| Rok vydání: | 2002 |
| Předmět: |
medicine.medical_specialty
Very low-density lipoprotein Apolipoprotein B Lipoproteins medicine.medical_treatment Hyperlipidemias Biochemistry Mice chemistry.chemical_compound Phospholipid transfer protein Internal medicine Cholesterylester transfer protein medicine Animals Humans Vitamin E Phospholipid Transfer Proteins Molecular Biology Phospholipids Triglycerides Mice Knockout Intermediate-density lipoprotein biology Membrane Proteins Cell Biology Kinetics Cholesterol Endocrinology Immunoglobulin M chemistry Immunoglobulin G Low-density lipoprotein biology.protein lipids (amino acids peptides and proteins) Ca(2+) Mg(2+)-ATPase Carrier Proteins Oxidation-Reduction Lipoprotein |
| Zdroj: | Journal of Biological Chemistry. 277:31850-31856 |
| ISSN: | 0021-9258 |
| Popis: | Vitamin E is a lipophilic anti-oxidant that can prevent the oxidative damage of atherogenic lipoproteins. However, human trials with vitamin E have been disappointing, perhaps related to ineffective levels of vitamin E in atherogenic apoB-containing lipoproteins. Phospholipid transfer protein (PLTP) promotes vitamin E removal from atherogenic lipoproteins in vitro, and PLTP deficiency has recently been recognized as an anti-atherogenic state. To determine whether PLTP regulates lipoprotein vitamin E content in vivo, we measured alpha-tocopherol content and oxidation parameters of lipoproteins from PLTP-deficient mice in wild type, apoE-deficient, low density lipoprotein (LDL) receptor-deficient, or apoB/cholesteryl ester transfer protein transgenic backgrounds. In all four backgrounds, the vitamin E content of very low density lipoprotein (VLDL) and/or LDL was significantly increased in PLTP-deficient mice, compared with controls with normal plasma PLTP activity. Moreover, PLTP deficiency produced a dramatic delay in generation of conjugated dienes in oxidized apoB-containing lipoproteins as well as markedly lower titers of plasma IgG autoantibodies to oxidized LDL. The addition of purified PLTP to deficient plasma lowered the vitamin E content of VLDL plus LDL and normalized the generation of conjugated dienes. The data show that PLTP regulates the bioavailability of vitamin E in atherogenic lipoproteins and suggest a novel strategy for achieving more effective concentrations of anti-oxidants in lipoproteins, independent of dietary supplementation. |
| Databáze: | OpenAIRE |
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