Lipid-Protein Interactions in High Density Lipoproteins

Assmann, Gerd; Brewer, H. Bryan

doi:10.1073/pnas.71.3.989

Cited by 89 publications

(30 citation statements)

References 36 publications

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“…[N-C3H3-choline]SPM (sp act 2.8 x 105 cpm./mol) was purified by silica-gel chromatography and subsequently used as sonicated dispersion for recombination with Apo A-II as previously described (16). Lipid-protein complexes were isolated by sequential ultracentrifugation between d = 1.063-1.21 g/ml and subsequent agarose-gel chromatography (16).…”

Section: Methodsmentioning

confidence: 99%

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Isolation and Characterization of an Abnormal High Density Lipoprotein in Tangier Disease

Assmann¹,

Herbert²,

Fredrickson³

et al. 1977

J. Clin. Invest.

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Section: Methodsmentioning

confidence: 99%

“…Lipid-protein complexes were isolated by sequential ultracentrifugation between d = 1.063-1.21 g/ml and subsequent agarose-gel chromatography (16). Ultracentrifugal and column fractions were analyzed for phospholipid by determination of radioactivity, and for protein by the method of Lowry et al (17).…”

Section: Methodsmentioning

confidence: 99%

Isolation and Characterization of an Abnormal High Density Lipoprotein in Tangier Disease

Assmann¹,

Herbert²,

Fredrickson³

et al. 1977

J. Clin. Invest.

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“…apo AI, the major protein component of HDL, is an important determinant of the concentration of HDL in human blood (2,3). Overexpression of human apo AI in transgenic mice resulted in increased plasma levels of small HDL particles comparable to human HDL 3 (4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Substitution of the carboxyl-terminal domain of apo AI with apo AII sequences restores the potential of HDL to reduce the progression of atherosclerosis in apo E knockout mice.

Holvoet¹,

Danloy²,

Deridder³

et al. 1998

J. Clin. Invest.

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HDL metabolism and atherosclerosis were studied in apo E knockout (KO) mice overexpressing human apo AI, a des-(190-243)-apo AI carboxyl-terminal deletion mutant of human apo AI or an apo AI-(1-189)-apo AII-(12-77) chimera in which the carboxyl-terminal domain of apo AI was substituted with the pair of helices of apo AII. HDL cholesterol levels ranked: apo AI/apo E KO ‫ف‬ apo AI-(1-189)-apo AII-(12-77)/apo E KO Ͼ Ͼ des-(190-243)-apo AI/apo E KO Ͼ apo E KO mice. Progression of atherosclerosis ranked: apo E KO Ͼ des-(190-243)-apo AI/apo E KO Ͼ Ͼ apo AI-(1-189)-apo AII-(12-77)/apo E KO ‫ف‬ apo AI/apo E KO mice. Whereas the total capacity to induce cholesterol efflux from lipid-loaded THP-1 macrophages was higher for HDL of mice overexpressing human apo AI or the apo AI/apo AII chimera, the fractional cholesterol efflux rate, expressed in percent cholesterol efflux/ g apolipoprotein/h, for HDL of these mice was similar to that for HDL of mice overexpressing the deletion mutant and for HDL of apo E KO mice. This study demonstrates that the tertiary structure of apo AI, e.g., the number and organization of its helices, and not its amino sequence is essential for protection against atherosclerosis because it determines HDL cholesterol levels and not cholesterol efflux. Amino acid sequences of apo AII, which is considered to be less antiatherogenic, can be used to restore the structure of apo AI and thereby its antiatherogenicity.

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“…The isolation was performed at 4°C with two ultracentrifugations only, 24 h at 1.09 gIml and 48 h at 1.21 g/ml at 39,000 rpm in a Beckman 40.3 rotor. The product was not washed with an additional ultracentrifugation at 1.21 g/ml in order to minimize preferential loss of apoA-I (11,13,15). Protein concentration was measured.…”

mentioning

confidence: 99%

“…It is rather loosely bound to HDL and can be separated from the rest of HDL by relatively mild procedures (11)(12)(13)(14). ApoA-II is associated with HDL lipid more tightly and therefore may play more of a structural role in the HDL particle (15). In man it is present as a dimer with a mol wt of 17,380 (9).…”

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confidence: 99%

High Density Lipoprotein Metabolism in Man

Blum¹,

Levy²,

Eisenberg³

et al. 1977

J. Clin. Invest.

382

115

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A B S T R A C T The turnover of 125I-high density lipoprotein (HDL) was examined in a total of 14 studies in eight normal volunteers in an attempt to determiine the metabolic relationship between apolipoproteins A-I (apoA-I) and A-II (apoA-II) of HDL and to define further some of the determinants of HDL metabolism. All subjects were first studied unider conditions of an isocaloric balanced diet (40% fat, 40% carbohydrate). Four were then studied with an 80% carbohydrate diet, and two were studied while receiving nicotinic acid (1 g three times daily) anid ingesting the same isocaloric balanced diet. The dlecay of autologous 1251-HDL and the appearance of urinary radioactivity were followed for at least 2 wk in each study. ApoA-I and apoA-II were isolated by Sephadex G-200 chromatography from serial plasma samples in each study. The specific activities of these peptides were then measured directly.It was found that the decay of specific activity of apoA-I and apoA-II were parallel to one another in all studies. The mean half-life of the terminal portion of decay was 5.8 days during the studies with a balanced diet.Mathematical modeling of the decay of plasma radioactivity and appearance of urinary radioactivity was most consistent with a two-compartment model. One compartment is within the plasma and exchanges with a nonplasma component. Catabolism occurs from both of these compartments.With a balanced isocaloric diet, the mean synthetic rate for HDL protein was 8.51 mg/kg per day. HDL synthesis was not altered by the high carbohydrate Dr. Blum's current address is the Department of Medicine, College ofPhysicians & Surgeons, Columbia University, New York 10032. Dr. Eisenberg's current address is the Department of Medicine B, Hadassah Hospital, Jerusalem, Israel.Reprint requests should be addressed to Robert I. Levy, M.D., National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, 20014. Receivedfor publication 7January 1977 given beginning 3 days before the injection of '25I-HDL, and ferrous sulfate, 300 mg, was given three times daily. The patients received no other medications. Informed consent was obtained.Collectiot of plasmrla. Blood was obtained in 0.1% EDTA, usually after an overnight fast (12-14 h), and the plasma was separated at 40C in a refrigerated centrifuge. In three instances during each turnover study, nonfastinig blood was obtained; these were at 6, 12, and 36 h after the 9:00 a.m. initiation of the studies.Isolation and labeling of HDL. Autologous HDL was isolated at 4°C over the density range 1.09-1.21 g/ml according to the method of Havel et al. (17). Successive ultracentrifugation was carried out in a Beckman 60 Ti rotor (Beckman Instruments, Inc., Fullerton, Calif.) at 59,000 rpm for 18 h at d 1.09 g/ml, and for 24 h at d 1.21 g/ml. The HDL thus obtained was resuspended in an NaCl-KBr solution of d 1.21 g/ml and washed by ultracentrifugation for 24 h at 64,000 rpm in a Beckman 65 rotor. KBr was then removed by at least four successive 30-min dialyses ...

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Lipid-Protein Interactions in High Density Lipoproteins

Cited by 89 publications

References 36 publications

Isolation and Characterization of an Abnormal High Density Lipoprotein in Tangier Disease

Isolation and Characterization of an Abnormal High Density Lipoprotein in Tangier Disease

Substitution of the carboxyl-terminal domain of apo AI with apo AII sequences restores the potential of HDL to reduce the progression of atherosclerosis in apo E knockout mice.

High Density Lipoprotein Metabolism in Man

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