Retroendocytosis of high density lipoproteins by the human hepatoma cell line, HepG2.

Kambouris, Ambrosios M.; Roach, Paul D.; Calvert, G. D.; Nestel, P.J.

doi:10.1161/01.atv.10.4.582

Cited by 51 publications

(30 citation statements)

References 37 publications

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“…There have been some reports arguing both for a non-endocytotic, cell surface mechanism (Pittman et al, 1987) that is supported by the intrinsic capacity of SR-BI to incorporate CE into membranes and an endocytotic mechanism involving retroendocytosis of HDL particles depleted of CE in mouse hepatocytes , which is also present in HepG2 cells (Kambouris et al, 1990). Our results favour the retroendocytosis model, which does not exclude a direct role for SR-BI in transferring CE to membranes.…”

Section: Discussionsupporting

confidence: 47%

“…Lipoprotein recycling (retroendocytosis) assays were conducted separately with both 125 I-lipoprotein and [ 3 H]CE-lipoprotein, by a pulse-chase protocol adapted from Kambouris et al (Kambouris et al, 1990) and Greenspan and St Clair (Greenspan and St Clair, 1984). Firstly, radiolabelled LDL (20 µg protein/ml), HDL3 (40 µg protein/ml) or M-BSA were incubated as described for the cell association assay, for 2 hours at 37°C in a 500 µl total volume (pulse phase).…”

Section: Lipoprotein Recycling (Retroendocytosis) Assaysmentioning

confidence: 99%

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Localization and regulation of SR-BI in membrane rafts of HepG2 cells

Rhainds

Bourgeois

Bourret

et al. 2004

Journal of Cell Science

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The scavenger receptor class B, type I (SR-BI) mediates cholesteryl esters (CE) selective uptake from low density lipoprotein (LDL) and high-density lipoprotein (HDL) particles. In a number of tissues expressing caveolin, SR-BI is localized in caveolae. We show using detergent-free sucrose gradients that SR-BI is found in membrane rafts devoid of caveolin-1 in the human hepatoma HepG2 cell. Perturbation of the structure of HepG2 cell membrane rafts with cholesterol oxidase or sphingomyelinase decreased LDL-CE association due to selective uptake by 60%, while HDL3-CE selective uptake was increased 2.3-fold by cholesterol oxidase but was not affected by sphingomyelinase. Sequestration of membrane cholesterol with filipin III decreased LDL-CE selective uptake by 25%, while it had no effect on HDL3-CE selective uptake. Extraction of cell membrane cholesterol with β-cyclodextrin increased LDL- and HDL3-CE selective uptake by 1.6-fold and 3-fold, respectively. We found that CE-selective uptake from both HDL and LDL occurs by a pathway involving retro-endocytosis in HepG2 cells. An analysis of the effect of SR-BI level on the expression of critical lipid sensor and lipid binding proteins was conducted with stable transformants of HepG2 cell overexpressing SR-BI. We found that liver-type fatty acid binding protein expression level is higher in SR-BI-overexpressing cells and that caveolin-1 and sterol response element binding protein-2 levels are reduced. Thus, in this hepatic cell model, SR-BI is associated with membrane rafts devoid of caveolin and its expression affects intracellular lipid binding and lipid sensor proteins. SR-BI-dependent LDL- and HDL-CE selective uptake are affected differently by the integrity of membrane rafts, but both occur by a retroendocytic pathway in HepG2 cells.

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Section: Discussionsupporting

confidence: 47%

Section: Lipoprotein Recycling (Retroendocytosis) Assaysmentioning

confidence: 99%

Localization and regulation of SR-BI in membrane rafts of HepG2 cells

Rhainds

Bourgeois

Bourret

et al. 2004

Journal of Cell Science

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“…However, these studies might have missed a rapid internalization of HDL and resecretion into the medium. Indeed, in various hepatoma cell lines, including HepG2 cells, a retroendocytic pathway for HDL has been described (7,8). Uptake of HDL was blocked by ATP depletion or by exposure to low temperature, and it was sensitive to agents interfering with endocytic recycling (8,28).…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have characterized a retroendocytic pathway for HDL in hepatocytes and hepatoma HepG2 cells by which internalized HDL has been proposed to recycle rapidly toward the basolateral membrane surface (6)(7)(8). By this process, HDL-associated lipids can be delivered to the hepatocyte (8).…”

mentioning

confidence: 99%

Different transport routes for high density lipoprotein and its associated free sterol in polarized hepatic cells

Wüstner¹,

Mondal

Huang

et al. 2004

Journal of Lipid Research

114

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“…Some authors have demonstrated resecretion of HDL, which was internalized into liver cells. 189,190 Interestingly, hepatic binding, uptake, degradation, and resecretion of HDL is disturbed in ob/ob mice, which are deficient in leptin. 191 Because ob/ob mice have elevated HDL-C levels because of retarded HDL catabolism, 192 Tall and colleagues have suggested the presence of a hepatic leptin-regulated HDL receptor, which regulates HDL-C levels by mediating holoparticle uptake into liver cells.…”

Section: Catabolism Of Hdl Apolipoproteinsmentioning

confidence: 99%

High Density Lipoproteins and Arteriosclerosis

Eckardstein

Nofer

Assmann

2001

ATVB

604

128

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Abstract-High density lipoprotein (HDL) cholesterol is an important risk factor for coronary heart disease, and HDL exerts various potentially antiatherogenic properties, including the mediation of reverse transport of cholesterol from cells of the arterial wall to the liver and steroidogenic organs. Enhancement of cholesterol efflux and of reverse cholesterol transport (RCT) is considered an important target for antiatherosclerotic drug therapy. Levels and composition of HDL subclasses in plasma are regulated by many factors, including apolipoproteins, lipolytic enzymes, lipid transfer proteins, receptors, and cellular transporters. In vitro experiments as well as genetic family and population studies and investigation of transgenic animal models have revealed that HDL cholesterol plasma levels do not necessarily reflect the efficacy and antiatherogenicity of RCT. Instead, the concentration of HDL subclasses, the mobilization of cellular lipids for efflux, and the kinetics of HDL metabolism are important determinants of RCT and the risk of atherosclerosis. (Arterioscler Thromb Vasc Biol. 2001;21:13-27.)

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Retroendocytosis of high density lipoproteins by the human hepatoma cell line, HepG2.

Cited by 51 publications

References 37 publications

Localization and regulation of SR-BI in membrane rafts of HepG2 cells

Localization and regulation of SR-BI in membrane rafts of HepG2 cells

Different transport routes for high density lipoprotein and its associated free sterol in polarized hepatic cells

High Density Lipoproteins and Arteriosclerosis

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