Comparison of various methods for in vitro cholesteryl ester labeling of lipoproteins from hypercholesterolemic rabbits

Hough, Jane L.; Zilversmit, D. B.

doi:10.1016/0005-2760(84)90202-9

Cited by 55 publications

(15 citation statements)

References 29 publications

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“…Determination of HDL Cholesteryl Ether Transport-Mouse HDL was isolated in the density range of 1.07-1.21 g/ml using sequential preparative ultracentrifugation and standard techniques (29) and labeled with either the intracellularly trapped [1␣,2␣-3 H]cholesteryl oleyl ether (18,30,31) or [cholesteryl-4-14 C]oleate by exchange from donor liposomes as described (13,32). Rates of HDL cholesteryl ether transport were determined using a primed infusion protocol as previously described (16).…”

Section: Methodsmentioning

confidence: 99%

Effect of Up-regulating Individual Steps in the Reverse Cholesterol Transport Pathway on Reverse Cholesterol Transport in Normolipidemic Mice

Alam

Meidell

Spady

2001

Journal of Biological Chemistry

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Cholesterol acquired by extrahepatic tissues (from de novo synthesis or lipoproteins) is returned to the liver for excretion in a process called reverse cholesterol transport (RCT). We undertook studies to determine if RCT could be enhanced by up-regulating individual steps in the RCT pathway. Overexpression of 7␣-hydroxylase, Scavenger receptor B1, lecithin:cholesterol acyltransferase (LCAT), or apoA-I in the liver did not stimulate cholesterol efflux from any extrahepatic tissue. In contrast, infusion of apoA-I⅐phospholipid complexes (rHDL) that resemble nascent HDL markedly stimulated cholesterol efflux from tissues into plasma. Cholesterol effluxed to rHDL was initially unesterified but by 24 h this cholesterol was largely esterified and had shifted to normal HDL (in mice lacking cholesteryl ester transfer protein) or to apoB containing lipoproteins (in cholesteryl ester transfer protein transgenic mice). Most of the cholesterol effluxed into plasma in response to rHDL came from the liver. However, an even greater proportion of effluxed cholesterol was cleared by the liver resulting in a transient increase in liver cholesterol concentrations. Fecal sterol excretion was not increased by rHDL. Thus, although rHDL stimulated cholesterol efflux from most tissues and increased net cholesterol movement from extrahepatic tissues to the liver, cholesterol flux through the entire RCT pathway was not increased.Cholesterol that has been acquired by extrahepatic tissues (from de novo synthesis or lipoproteins) is returned to the liver for excretion in a process called reverse cholesterol transport (RCT) 1 (1-3). The first step in the RCT pathway is efflux of cholesterol from cell membranes to nascent HDL in interstitial fluid (2, 3). Nascent HDL are discoidal pre-␤-migrating complexes of phospholipid and apoA-I (other amphipathic apoproteins such as apoE and apoA-IV may also be present). These particles are secreted by the liver (4, 5) and small intestine (6) and are also formed during the metabolism of triglyceride-rich lipoproteins from excess surface material. In addition, lipid-free apoA-I can mediate the efflux of cholesterol and phospholipid from cells generating pre␤-migrating nascent HDL (7,8). ATP-binding cassette transporter 1 (ABCA1) appears to play a key role in this process although the exact mechanism is unclear (9 -12). Cholesterol that is transferred to nascent HDL is esterified by lecithin: cholesterol acyltransferase (LCAT) to cholesteryl esters, which by virtue of their hydrophobicity move into the core of the HDL particle resulting in the formation of ␣-migrating spherical HDL. HDL cholesteryl esters are cleared from plasma mainly by the liver (13-16). HDL cholesteryl ester uptake by the liver is mediated by the scavenger receptor BI (SR-BI), which selectively transports HDL cholesteryl esters resulting in an HDL particle of reduced size and cholesteryl ester content (17, 18). In species with cholesteryl ester transfer protein, a portion of HDL cholesteryl ester is transferred to lower density apoB-c...

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Section: Methodsmentioning

confidence: 99%

Effect of Up-regulating Individual Steps in the Reverse Cholesterol Transport Pathway on Reverse Cholesterol Transport in Normolipidemic Mice

Alam

Meidell

Spady

2001

Journal of Biological Chemistry

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“…Hamster HDL ( d ϭ 1.07-1.21 g/ml) was isolated as described above and labeled with either the intracellularly trapped [1 ␣ , 2 ␣ (n)- C]oleate by exchange from donor liposomes as described (11,28). Freshly collected rabbit plasma or a d Ͼ 1.21 g/ml fraction of rabbit plasma was used as a source of CETP (11).…”

Section: Methodsmentioning

confidence: 99%

Kinetic parameters for high density lipoprotein apoprotein AI and cholesteryl ester transport in the hamster.

Woollett

Spady²

1997

J. Clin. Invest.

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These studies were undertaken to determine the kinetic characteristics of high density lipoprotein (HDL) apo AI and cholesteryl ester transport in the hamster in vivo. Saturable HDL apo AI transport was demonstrated in the kidneys, adrenal glands, and liver. Saturable HDL cholesteryl ester transport was highest in the adrenal glands and liver. In the liver and adrenal glands, maximal transport rates ( J m ) for receptor dependent uptake were similar for the protein and cholesteryl ester moieties; however, the concentration of HDL necessary to achieve half-maximal transport ( K m ) was 20-to 30-fold higher for apo AI. Consequently, at normal plasma HDL concentrations, the clearance of HDL cholesteryl ester exceeded that of HDL apo AI by ‫ف‬ 10-fold in the adrenal glands and by approximately fivefold in the liver. At normal HDL concentrations, the majority of HDL cholesteryl ester (76%) was cleared by the liver whereas the majority of HDL apo AI (77%) was cleared by extrahepatic tissues. The rate of HDL cholesteryl ester uptake by the liver equaled the rate of cholesterol acquisition by all extrahepatic tissues suggesting that HDL cholesteryl ester uptake by the liver accurately reflects the rate of "reverse cholesterol transport." Receptor dependent HDL cholesteryl ester uptake by the liver was maximal (

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“…After dialysis, these radiolabeled preparations were passed through a 0.45 mm Millex-HA filter immediately prior to injection into the recipient animals. HDL-C was labeled with either the intracellularly trapped [1a, 2a(n)- 3 H]cholesteryl oleyl ether or [cholesteryl-4-14 C]oleate by exchange from donor liposomes as described (31)(32)(33). Freshly collected plasma from cholesteryl ester transfer protein transgenic mice was used as a source of CETP.…”

Section: Isolation and Radiolabeling Of Ldl And Hdlmentioning

confidence: 99%

ABCA1 plays no role in the centripetal movement of cholesterol from peripheral tissues to the liver and intestine in the mouse

Xie

Turley

Dietschy

2009

Journal of Lipid Research

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This study uses the mouse to explore the role of ABCA1 in the movement of this cholesterol from the peripheral organs to the endocrine glands for hormone synthesis and liver for excretion. The sterol pool in all peripheral organs was constant and equaled 2,218 and 2,269 mg/kg, respectively, in abca1 1/1 and abca1 2/2 mice. Flux of cholesterol from these tissues equaled the rate of synthesis plus the rate of LDL-cholesterol uptake and was 49.9 mg/day/kg in control animals and 62.0 mg/day/kg in abca1 2/2 mice. In the abca1 1/1 animals, this amount of cholesterol moved from HDL into the liver for excretion. In the abca1 2/2 mice, the cholesterol from the periphery also reached the liver but did not use HDL. Fecal excretion of cholesterol was just as high in abac1 2/2 mice (198 mg/day/kg) as in the abac1animals (163 mg/day/kg), although the abac1 2/2 mice excreted relatively more neutral than acidic sterols. This study established that ABCA1 plays essentially no role in the turnover of cholesterol in peripheral organs or in the centripetal movement of this sterol to the endocrine glands, liver, and intestinal tract for excretion.-Xie, C., S. D. Turley, and J. M. Dietschy. ABCA1 plays no role in the centripetal movement of cholesterol from peripheral tissues to the liver and intestine in the mouse. J. Lipid Res. 2009Res. . 50: 1316Res. -1329

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Comparison of various methods for in vitro cholesteryl ester labeling of lipoproteins from hypercholesterolemic rabbits

Cited by 55 publications

References 29 publications

Effect of Up-regulating Individual Steps in the Reverse Cholesterol Transport Pathway on Reverse Cholesterol Transport in Normolipidemic Mice

Effect of Up-regulating Individual Steps in the Reverse Cholesterol Transport Pathway on Reverse Cholesterol Transport in Normolipidemic Mice

Kinetic parameters for high density lipoprotein apoprotein AI and cholesteryl ester transport in the hamster.

ABCA1 plays no role in the centripetal movement of cholesterol from peripheral tissues to the liver and intestine in the mouse

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