Transfers and exchanges of esterified cholesterol between plasma lipoproteins

Barter, Philip J.; Hopkins, Garry J.; Calvert, G. D.

doi:10.1042/bj2080001

Cited by 182 publications

(71 citation statements)

References 53 publications

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“…This widely distributed protein, recently identified by ourselves [12, 211 and other groups [19,22,231, is considered to have a role, as yet ill-defined, in lipid metabolism. One suggestion is that apo J is part of a lipid transfer complex [19]; lipid transfer activity is an important facet of the process which channels excess cholesterol to the liver for eventual excretion [39,40]. Another prominent feature of the lipid composition of the fraction bound by anti-(K-45) is its high triacylglycerol content.…”

Section: Discussionmentioning

confidence: 99%

Identification of a distinct human high‐density lipoprotein subspecies defined by a lipoprotein‐associated protein, K‐45

Blatter

James

Messmer

et al. 1993

European Journal of Biochemistry

322

188

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In an attempt to provide immunological tools for subfractionation of high-density lipoproteins (HDL), monoclonal antibodies were raised against HDL complexes. Two clones identified a peptide, provisionally named K-45 (PI 4.5-4.9; molecular mass 45 kDa, range 42-48 kDa), whose plasma distribution and lipoprotein association were fully characterised. Gel filtration localised the peptide to the HDL region of human plasma where it co-eluted with apolipoprotein (apo) A-I, the structural protein of HDL. Complementary studies employing immunoabsorption with anti-(apo A-I) antibodies removed 90 % of K-45 from plasma: conversely, anti-(apo A-11) antibodies eliminated only 10 % of K-45. Immunoaffinity chromatography on an anti-(K-45) column revealed that the peptide was present in a distinct HDL subspecies containing three major proteins: K-45, apo A-I and clusterin or apo J. The lipoprotein nature of the bound fraction was indicated by electron microscopy (diameter 9.6 ? 3.3 nm) and quantification of lipids, the latter showing an unusually high triacyglycerol concentration. Plasma concentrations of K-45 were positively correlated with apo A-I and HDL-cholesterol and negatively correlated with apo B and total cholesterol. Thus, the peptide appears to be linked, directly or indirectly, to processes which give rise to an anti-atherogenic lipid profile. After completion of the present studies, an N-terminal sequence identical to that of K-45 was reported in recently isolated cDNA clones. These clones encode paraoxonase.Lipoprotein complexes are the principal transport vehicles for plasma lipids. As such, they are the focus of particular attention which derives from the designation of blood lipids as primary cardiovascular risk factors [l, 21. The rationale behind these studies is that a dysfunctional lipid transport system will be a major cause of the dyslipidaemias associated with premature cardiovascular disease [3]. In this context, an obvious pre-requisite is a comprehensive understanding of the normal functioning of the lipoprotein metabolic system ; unfortunately, this is not currently the case. It is due, in part, to the highly dynamic nature of this metabolic process, rendered even more intricate by extensive interactions between the major subclasses, very-low-density (VLDL), low-density (LDL) and high-density (HDL) lipoproteins [4]. The latter are of particular interest as they afford a measure of protection against cardiovascular disease [5, 61. Yet many aspects of HDL metabolism are poorly understood. Neither the origins nor the sites of catabolism of this lipoprotein species have been convincingly demonstrated. Additionally, the mechanisms by which HDL assure their postuCorrespondence to R.

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Section: Discussionmentioning

confidence: 99%

Identification of a distinct human high‐density lipoprotein subspecies defined by a lipoprotein‐associated protein, K‐45

Blatter

James

Messmer

et al. 1993

European Journal of Biochemistry

322

188

View full text Add to dashboard Cite

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“…With reduced CE formation, combined with a marked decrease of the plasma pool of normal HDL, the transfer of CE to VLDL may also be impaired. 42 The exchange of CE and TG will occur predominantly between VLDL and LDL, 43 with consequent formation of TG-rich and CE-poor LDL in plasma. 12 By these mechanisms, A-I M + subjects with HTG may represent the final result of a series of events where a progressive derangement of the complex pathways regulating the interaction between HDL and TG-rich lipoproteins may take place accounting for the appearance of hypertriglyceridemia in the older A-I M + subjects.…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein A-IMilano. Correlation between high density lipoprotein subclass distribution and triglyceridemia.

Franceschini¹,

Calabresi²,

Tosi³

et al. 1987

Arteriosclerosis

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Carriers of the apolipoprotein A-I unino (apo A-I M ) variant represent a selected group of subjects showing low levels of high density lipoprotein (HDL), variable hypertrlglycerldemia, and low prevalence of atherosclerotic vascular disease. The distribution of HDL subtractions and the correlation with abnormalities in triglycerlde transport were determined In these subjects. Sera from 24 apo A-I M carriers (A-I H + and from age-and sex-matched normollpldemlc controls (A-I u~) were analyzed by rate zonal ultracentrlrugatlon. The A-I H + subjects showed a marked decrease of HDL 3 mass with reduced flotation rates and major compositional alterations; the HDL 2 were nearly absent The HDL subclasses from 10 A-I u + subjects were resolved according to particle size by gradient gel eiectrophoresis (GGE). The HDL patterns detected In the carriers were unique In exhibiting a distinct peak In the (HDLuJgg, interval, undetectable In the controls. Three patterns reflecting the relative contributions of smaller (HDLjJgg. and larger (HDLj.)™ particles could be distinguished In the carriers, and these were clearly related to different triglycerlde and HDL cholesterol levels in plasma. These findings In a highly selected group of subjects with generally low HDL levels and quite variable triglyceridemia confirmed the existence of relationships between alterations In triglycerlde transport and abnormalities In the HDL subclass distribution, possibly reflecting the variable atherosclerotic risk in hypertrlglycerldemlc subjects. (Arteriosclerosis 7:426-435, July/August 1987)

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“…Figure 3C illustrates that HDL cholesteryl ester as percentage of plasma declined after an oral fat load from 10% (6-11) to 8% (4-11), p<0.05, analyzed from 0 to 8 hours. LDL and TRL cholesteryl ester did not change significantly from 8 1 % (78-88) to 82% (79-88), and from 10% (5-12) to 11% (5)(6)(7)(8)(9)(10)(11)(12)(13)(14), respectively.…”

Section: Cholesteryi Ester Distribution Between Upoprotelnsmentioning

confidence: 99%

Alimentary lipemia-induced redistribution of cholesteryl ester between lipoproteins. Studies in normolipidemic, combined hyperlipidemic, and hypercholesterolemic men.

et al. 1989

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Transfers and exchanges of esterified cholesterol between plasma lipoproteins

Cited by 182 publications

References 53 publications

Identification of a distinct human high‐density lipoprotein subspecies defined by a lipoprotein‐associated protein, K‐45

Identification of a distinct human high‐density lipoprotein subspecies defined by a lipoprotein‐associated protein, K‐45

Apolipoprotein A-IMilano. Correlation between high density lipoprotein subclass distribution and triglyceridemia.

Alimentary lipemia-induced redistribution of cholesteryl ester between lipoproteins. Studies in normolipidemic, combined hyperlipidemic, and hypercholesterolemic men.

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