Clathrin-mediated endocytosis of high density lipoprotein3 in human intestinal Caco-2 cells. A post-embedding immunocytochemical study

Klinger, Antje; Reimann, Frank; Klinger, Matthias; Stange, Eduard F.

doi:10.1016/s0005-2760(96)00164-6

Cited by 11 publications

(6 citation statements)

References 26 publications

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“…SR-BI is abundantly expressed in liver and steroidogenic tissues but has not been found in brain (81), and we were unable to detect SR-BI in sympathetic neurons. In addition to selective lipid uptake from HDL, the endocytosis and lysosomal degradation of HDL holoparticles have previously been observed (53,54). In our experiments, not only lipids but also proteins of hHDL 3 were internalized by axons and transported to cell bodies, indicating holoparticle uptake.…”

Section: Figsupporting

confidence: 75%

“…Our findings also confirm that the various lipoprotein classes are differentially taken up by cell bodies and distal axons of sympathetic neurons. Previous studies have reported that in several cell types a selective uptake of lipids, particularly cholesteryl esters, occurs from HDL (43), whereas the uptake of HDL holoparticles has been less well documented (53,54). Therefore, our observation that distal axons of sympathetic neurons were able to internalize both lipids and proteins from hHDL 3 was somewhat unexpected.…”

Section: Resultsmentioning

confidence: 49%

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Uptake of Lipoproteins for Axonal Growth of Sympathetic Neurons

Chaves¹,

Vance²,

Campenot³

et al. 2000

Journal of Biological Chemistry

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Lipoproteins originating from axon and myelin breakdown in injured peripheral nerves are believed to supply cholesterol to regenerating axons. We have used compartmented cultures of rat sympathetic neurons to investigate the utilization of lipids from lipoproteins for axon elongation. Lipids and proteins from human low density lipoproteins (LDL) and high density lipoproteins (HDL) were taken up by distal axons and transported to cell bodies, whereas cell bodies/proximal axons internalized these components from only LDL, not HDL. Consistent with these observations, the impairment of axonal growth, induced by inhibition of cholesterol synthesis, was reversed when LDL or HDL were added to distal axons or when LDL, but not HDL, were added to cell bodies. LDL receptors (LDLRs) and LR7/8B (apoER2) were present in cell bodies/proximal axons and distal axons, with LDLRs being more abundant in the former. Inhibition of cholesterol biosynthesis increased LDLR expression in cell bodies/proximal axons but not distal axons. LR11 (SorLA) was restricted to cell bodies/proximal axons and was undetectable in distal axons. Neither the LDL receptor-related protein nor the HDL receptor, SR-B1, was detected in sympathetic neurons. These studies demonstrate for the first time that lipids are taken up from lipoproteins by sympathetic neurons for use in axonal regeneration.Axonal elongation requires the expansion of axonal membranes by addition of new membrane materials (proteins and lipids) to the growing axon. In sheep (1) and rats (2, 3) the brain and peripheral nerves synthesize all the cholesterol needed for development without requiring cholesterol from circulating lipoproteins. Moreover, after birth, cholesterol used for myelin production is made locally (4). In contrast, fetal liver supplies about 50% of the cholesterol needed for development of heart, lung, and kidney (3). Surprisingly, during peripheral nerve regeneration, cholesterol synthesis in the nerve is down-regulated (5), yet serum-derived cholesterol does not contribute significantly to myelin synthesis or axonal regeneration (6, 7).Instead, cholesterol from degenerating axons and myelin is proposed to be retained within the nerve and re-utilized via a lipoprotein-mediated process (8), although cholesterol uptake by neurons was not directly demonstrated. The presence of endoneural lipoproteins in regenerating, but not non-injured, nerves is well documented. These lipoproteins contain apolipoprotein (apo) 1 E and apoAI but not apoB (9 -11). After peripheral nerve injury, apoE synthesis by resident macrophages increases greatly, and apoE accumulates within the nerve (12-14) supporting the concept that apoE is involved in re-utilization of lipids from degenerating nerves for axonal regeneration and myelin production.The receptors involved in lipoprotein uptake by axons and Schwann cells have not been fully characterized, nor has the uptake and utilization of lipids from lipoproteins for axonal regeneration been directly demonstrated. The low density lipoprotein receptor...

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Section: Figsupporting

confidence: 75%

Section: Resultsmentioning

confidence: 49%

Uptake of Lipoproteins for Axonal Growth of Sympathetic Neurons

Chaves¹,

Vance²,

Campenot³

et al. 2000

Journal of Biological Chemistry

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“…In line with this observation, HDL is efficiently endocytosed via clathrin-coated pits in HepG2 cells, a cell line devoid of plasma membrane caveolae [44,45]. HDL endocytosis is also clathrin-mediated in Caco-2 cells [46]. Indeed, the caveolar density remarkably differs in different tissues.…”

Section: Intracellular Hdl Trafficking and Lipid Exchangementioning

confidence: 84%

HDL endocytosis and resecretion

Röhrl

Stangl

2013

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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HDL removes excess cholesterol from peripheral tissues and delivers it to the liver and steroidogenic tissues via selective lipid uptake without catabolism of the HDL particle itself. In addition, endocytosis of HDL holo-particles has been debated for nearly 40 years. However, neither the connection between HDL endocytosis and selective lipid uptake, nor the physiological relevance of HDL uptake has been delineated clearly. This review will focus on HDL endocytosis and resecretion and its relation to cholesterol transfer. We will discuss the role of HDL endocytosis in maintaining cholesterol homeostasis in tissues and cell types involved in atherosclerosis, focusing on liver, macrophages and endothelium. We will critically summarize the current knowledge on the receptors mediating HDL endocytosis including SR-BI, F1-ATPase and CD36 and on intracellular HDL transport routes. Dependent on the tissue, HDL is either resecreted (retro-endocytosis) or degraded after endocytosis. Finally, findings on HDL transcytosis across the endothelial barrier will be summarized. We suggest that HDL endocytosis and resecretion is a rather redundant pathway under physiologic conditions. In case of disturbed lipid metabolism, however, HDL retro-endocytosis represents an alternative pathway that enables tissues to maintain cellular cholesterol homeostasis.

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“…Garcia et al (20) reported that HDL was taken up into clathrin-coated vesicles by HepG2 cells, in a process that was inhibited by sucrose hypertonic shock. HDL uptake by Caco-2 cells also occurs via clathrin-mediated endocytosis (21), and HDL retroendocytosis also is detected in these cells (22). There is also evidence of non-HDL apoE recycling and resecretion after the uptake of triglyceride-rich lipoproteins, or reconstituted proteoliposomes containing only apoE, into Hep3b cells (23).…”

Section: Discussionmentioning

confidence: 99%

Cholesterol efflux to apolipoprotein AI involves endocytosis and resecretion in a calcium-dependent pathway

Takahashi

Smith

1999

Proc. Natl. Acad. Sci. U.S.A.

225

171

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We previously have described the cAMPmediated induction of cholesterol and phospholipid eff lux from the murine macrophage RAW264 cell line to lipid-free apolipoprotein acceptors. This induction of cholesterol eff lux is associated with increased binding and association of apolipoprotein to the cells. In the present study, using primarily apolipoprotein AI (apoAI) as the acceptor, cAMP-dependent cholesterol eff lux to apolipoprotein acceptors was associated with apoAI binding to coated pits, cellular uptake, and resecretion. After cell association and washing, 58% of the apoAI was resecreted during a 90-min chase period. In addition, after apoAI uptake and washing, cholesterol eff lux was observed during a chase period without additional acceptors. Cholesterol eff lux was partially blocked by chlorpromazine and hypertonic media, two inhibitors of coated pit endocytosis. Cholesterol eff lux to apoAI was found to depend on extracellular calcium. By temporally separating the cAMP induction phase from the apoAI chase phase, calcium was found to be required during the apoAI chase phase rather than during the cAMP induction period. In the absence of calcium the 8-Br-cAMP-mediated induction of apoAI binding was maintained, but the specific apoAI cellular association was inhibited. The data are consistent with a model for cholesterol eff lux to apolipoproteins that involves a calcium-dependent endocytic pathway, followed by recycling and the subsequent release of the nascent lipoprotein particle from the cell.

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Clathrin-mediated endocytosis of high density lipoprotein3 in human intestinal Caco-2 cells. A post-embedding immunocytochemical study

Cited by 11 publications

References 26 publications

Uptake of Lipoproteins for Axonal Growth of Sympathetic Neurons

Uptake of Lipoproteins for Axonal Growth of Sympathetic Neurons

HDL endocytosis and resecretion

Cholesterol efflux to apolipoprotein AI involves endocytosis and resecretion in a calcium-dependent pathway

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