The Interaction of Heparin with an Apoprotein of Human Very Low Density Lipoprotein

Shelburne, F; Quarfordt, Steven H.

doi:10.1172/jci108849

Cited by 199 publications

(57 citation statements)

References 29 publications

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“…Q total mass ratio of 2.1 ± 1.4 (retained vs. unretained VLDL) was obtained. The protein of the unretained VLDL fraction contained <0.1% apo E (as measured by radial immunodiffusion), which is comparable to previous reports (31,32). Only the latter is retained under the fractionation conditions described here.…”

Section: Resultssupporting

confidence: 91%

Plasma cholesterol metabolism in end-stage renal disease. Difference between treatment by hemodialysis or peritoneal dialysis.

Dieplinger¹,

Schoenfeld²,

Fielding³

1986

J. Clin. Invest.

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Plasma cholesterol metabolism was investigated in normotriglyceridemic patients with end-stage renal disease treated by hemo-or continuous ambulatory peritoneal dialysis (CAPD), and compared with that in a control group with normal renal function. A reversed net transport of free cholesterol from plasma to cultured fibroblasts, as well as greatly reduced levels of plasma cholesterol esterification and cholesterol ester transfer rates to low and very low density lipoproteins (LDL and VLDL), was found in the hemodialysis group compared to the controls. The LDL and VLDL contained increased amounts of free cholesterol and inhibited cholesterol ester transfer when recombined with control plasma. The LDL triglyceride content was doubled in the hemodialysis group, whereas cholesterol esters were decreased. Patients treated by CAPD, in marked contrast, had cholesterol metabolic rates that were within the normal range, as well as normal lipoprotein composition.

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Section: Resultssupporting

confidence: 91%

Plasma cholesterol metabolism in end-stage renal disease. Difference between treatment by hemodialysis or peritoneal dialysis.

Dieplinger¹,

Schoenfeld²,

Fielding³

1986

J. Clin. Invest.

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“…22 The purified apo E was injected into a female goat and plasma was obtained by plasma-phoresis at weekly intervals. Goat antibody to rat apo E was affinity-enriched by the absorption of the immune goat plasma to a rat HDL-Sepharose column as described by Hay and Getz.…”

Section: Antibody Preparationmentioning

confidence: 99%

Apoprotein E biosynthesis in the cholesterol-fed guinea pig.

et al. 1990

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Apoprotein E biosynthesis was evaluated In the livers of guinea pigs fed chow, 1% cholesterol plus 5% corn oil, or 1% cholesterol plus 5% coconut oil for a period of 12 weeks. Hypercholesterolemla was Induced by both experimental diets, although the coconut-oil diet resulted in higher levels. The ratios of free cholesterol/ cholesterol ester and of free cholesterol/total phosphollpid increased In the plasma of these animals. Peak lipid levels were mostly achieved by 8 weeks of diet Both cholesterol and triglyceride were substantially increased In the liver of animals fed the experimental diets, while phospholipid content was unchanged. The amount of apoprotein E mRNA In the guinea pig livers was evaluated by cell free translation assays and by membrane hybridization. The livers of animals fed corn oil with cholesterol for 4 weeks or 8 weeks contained 2 to 2.5 more apoprotein E mRNA compared to the control livers. With the diet containing coconut oil with cholesterol, the hepatic apoprotein E mRNA Increased somewhat later, so that by 8 weeks It was 1.7-to 1.9-fold higher than in the control animals. We conclude that high cholesterol diets, when fed as part of a high saturated or polyunsaturated fat diet, lead to Increased hepatic apo E mRNA abundance. The relationship between the Increased apo E mRNA levels and the previously described Increases in apo E synthesis and circulating apo E levels Is discussed. (Arteriosclerosis 10:31-39, January/February 1990)A polipoprotein E (apo E) is a 35 000 dalton glycoprctein found in many classes of mammalian plasma lipoproteins.1 Apo E is important in the metabolism of cholesterol-ester rich lipoproteins by virtue of its interaction with at least two lipoprotein receptor systems, the LDL receptor and the chylomicron remnant receptor.23 Plasma levels of apo E increase in a variety of circumstances, including diabetes, hypothyroidism, and cholesterol feeding. 46 In several species, cholesterol feeding leads to the appearance of new lipoproteins, /3-VLDL and HDLc, both of which are rich in cholesterol ester and epo E. The guinea pig has an unusual response to cholesterol feeding. In the normal guinea pig, the bulk of the plasma cholesterol is carried by low density lipoprotein (LDL), with high density lipoprotein (HDL) transporting less than 5% of the total cholesterol. 67 When guinea pigs are fed a diet supplemented with 1% cholesterol and 5% com or cottonseed oil, their plasma cholesterol levels increase from less than 100 mg/dl to 300 mg/dl within 10 days.68 Dietary

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“…Apolipoprotein A-| was isolated from HDL [25]. Apolipoprotein E was isolated from human VLDL by chromatography on heparin-Sepharose [26]. Apolipoprotein A-I and apolipoprotein E were homogeneous as determined by polyacrylamide gel electrophorsis in sodium dodecyl sulfate [27] and by amino acid analysis.…”

Section: Isolation Of Lipoproteins and Apoproteins Vldlmentioning

confidence: 99%

Interaction of a human plasma lipid transfer protein complex with lipid monolayers

Harmony

Jackson

Ihm

et al. 1982

Biochimica et Biophysica Acta (BBA) - Biomembranes

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The interaction of a purified human plasma lipid transfer complex with cholesteryl ester, triacylglycerol and phosphatidylcholine in binary and ternary lipid monolayers was investigated. The lipid transfer complex, designated LTC, catalyzes the removal of cholesteryl oleate and triacylglycerol from phosphatidylcholine monolayers. Preincuhation of LTC with p-chloromercuriphenyl sulfonate inhibits LTC-catalyzed removal of triacylglycerol; cholesteryl ester removal is not affected. The rate of LTC-facilitated removal of cholesteryl oleate from a phosphatidylcholine monolayer depends on the amount of LTC added to the subphase up to 100 p g protein. In addition, the rate of the LTC-catalyzed transfer of cholesteryl oleate to the subphase increases linearly as the amount of cholesteryl oleate in the monolayer increases to 6 mol%. LTC also removes cholesterol from phosphatidylcholine-cholesterol monolayers, albeit at a rate which is 15% of that for removal of cholesteryl oleate. The ability of LTC to facilitate triacyiglyceroi and cholesteryl ester removal depends on the composition of the monolayer. Phosphatidylcholine supports cholesteryl ester transfer whereas sphingomyelin-cholesteryi ester monolayers are almost refractory to LTC. In contrast, LTC removes triacylglycerol from either a phosphatidylcholine or a sphingomyelin monolayer. The results suggest the existence of at least two lipid transfer proteins, one of which catalyzes the removal of cholesteryl ester and the other triacylglycerol. The role of these proteins as they relate to lipoprotein metabolism is discussed.

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The Interaction of Heparin with an Apoprotein of Human Very Low Density Lipoprotein

Cited by 199 publications

References 29 publications

Plasma cholesterol metabolism in end-stage renal disease. Difference between treatment by hemodialysis or peritoneal dialysis.

Plasma cholesterol metabolism in end-stage renal disease. Difference between treatment by hemodialysis or peritoneal dialysis.

Apoprotein E biosynthesis in the cholesterol-fed guinea pig.

Interaction of a human plasma lipid transfer protein complex with lipid monolayers

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