The role of lipoprotein lipase and apoprotein E in the recognition of chylomicrons and chylomicron remnants by cultured isolated mouse hepatocytes

Chang, Suyi; Maeda, Nobuyo; Borensztajn, Jayme

doi:10.1042/bj3180029

Cited by 17 publications

(12 citation statements)

References 34 publications

(40 reference statements)

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“…The cellular response of hepatic apoA-I mRNA elicited by the different diets points out that remnants are taken by the liver through an apoE-independent mechanism, as suggested by Chang et al [31][32] and Quarfordt et al 33 and poses an exciting question regarding the ligand that facilitates the uptake in these conditions. Induction of the hepatic transgene cholesterol ester transfer proteins expression in apoE-null mice in response to dietary cholesterol has been reported by MasucciMagoulas et al 34 Their results and ours clearly show that transcription machinery in animals lacking apoE ligand is sensitive to dietary manipulations.…”

Section: Discussionmentioning

confidence: 94%

Low-Cholesterol and High-Fat Diets Reduce Atherosclerotic Lesion Development in ApoE-Knockout Mice

Calleja¹,

Paris²,

Paul³

et al. 1999

ATVB

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Abstract-We have investigated the effect of most common oils used in human nutrition on the development of atherosclerosis in apoE-knockout mice. Seven groups of animals, separated according to sex, were fed for 10 weeks either chow diet or the chow diet 10% (wt/wt) enriched with different oils (palm, coconut, 2 types of olive oil, and 2 types of sunflower oil) without addition of cholesterol. At the end of this period, plasma lipid parameters were measured and vascular lesions scored. None of the diets induced changes in plasma cholesterol concentrations, whereas plasma triglycerides were uniformly reduced in all diet groups. Some diets caused significant reductions in the size of atherosclerotic lesions in males and others in females; males responded most to sunflower oils and females to palm oil and one olive oil (II). The lesion reduction in males consuming sunflower oils was associated with the decrease of triglycerides in triglyceride-rich lipoproteins, whereas the decrease in females consuming olive oil II or palm oil was accompanied by an increase in plasma apoA-I. The increase in plasma apoA-I in the latter condition, is mainly due to overexpression of hepatic message elicited by a mechanism independent of apoE ligand. The data suggest that the different diets modulate lesion development in a gender specific manner and by different mechanisms and that the development of atherosclerosis, due to genetic deficiencies, may be modulated by nutritional maneuvers that may be implemented in human nutrition.

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Section: Discussionmentioning

confidence: 94%

Low-Cholesterol and High-Fat Diets Reduce Atherosclerotic Lesion Development in ApoE-Knockout Mice

Calleja¹,

Paris²,

Paul³

et al. 1999

ATVB

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“…Although LPL is synthesized in extrahepatic tissues, it circulates in blood in association with lipoproteins and is cleared by the liver (45,46). Several studies have shown that LPL enhances the binding and uptake of lipoproteins by cultured hepatoma cells and hepatocytes (6,7,38) and enhances the uptake of lipoproteins and lipid emulsions in perfused rat livers (40). LPL can bind to at least three plasma membrane receptors (6): (i) heparan sulfate proteoglycans, the most abundant and widely expressed LPL-binding molecules present at the surfaces of most cells; (ii) the ␣2-macroglobulin receptor/ low-density lipoprotein receptor-related protein (LRP); and (iii) other members of the LDL receptor family, such as the LDL receptor, the VLDL receptor, and GP330/LRP2.…”

Section: Discussionmentioning

confidence: 99%

“…LPL is synthesized in extrahepatic tissues (27,37) and circulates in the blood in association with lipoproteins (45). LPL has been proposed to play an important role in the clearance of triacylglycerol-rich lipoproteins and chylomicron remnants by hepatocytes through bridging lipoproteins to cell surface receptors (6,7,38,46). In view of the in vivo biological relevance of LPL, we addressed the question of whether LPL could play a role as an extrahepatic carrier in bridging HBV virions to the cell surface during viral infection.…”

Section: Fig 2 Gst Pull-down Assays For the Verification Of Presmentioning

confidence: 99%

“…As shown in Fig. 5B, GSTLPLc could interact with MBP-PreS1 1-65 (lane 3) but not PreS1 [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] (lane 4). The PreS-binding ability was lost in GSTLPLcm, where two tryptophan residues (aa 393 and 394) in the PreS-binding motif were mutated (lane 5).…”

Section: Fig 2 Gst Pull-down Assays For the Verification Of Presmentioning

confidence: 99%

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Identification and Characterization of Peptides That Interact with Hepatitis B Virus via the Putative Receptor Binding Site

Deng

Zhai

Michel

et al. 2007

J Virol

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A direct involvement of the PreS domain of the hepatitis B virus (HBV) large envelope protein, and in particular amino acid residues 21 to 47, in virus attachment to hepatocytes has been suggested by many previous studies. Several PreS-interacting proteins have been identified. However, they share few common sequence motifs, and a bona fide cellular receptor for HBV remains elusive. In this study, we aimed to identify PreS-interacting motifs and to search for novel HBV-interacting proteins and the long-sought receptor. PreS fusion proteins were used as baits to screen a phage display library of random peptides. A group of PreS-binding peptides were obtained. These peptides could bind to amino acids 21 to 47 of PreS1 and shared a linear motif (W 1 T 2 X 3 W 4 W 5 ) sufficient for binding specifically to PreS and viral particles. Several human proteins with such a motif were identified through BLAST search. Analysis of their biochemical and structural properties suggested that lipoprotein lipase (LPL), a key enzyme in lipoprotein metabolism, might interact with PreS and HBV particles. The interaction of HBV with LPL was demonstrated by in vitro binding, virus capture, and cell attachment assays. These findings suggest that LPL may play a role in the initiation of HBV infection. Identification of peptides and protein ligands corresponding to LPL that bind to the HBV envelope will offer new therapeutic strategies against HBV infection.Attachment of virions to human hepatocyte membrane via the interaction of the viral envelope protein with a specific cell surface receptor is considered the initial step of hepatitis B virus (HBV) infection. Besides host-derived phospholipids, the envelope of an HBV virion contains virus-derived small (SHBs), middle (MHBs), and large (LHBs) surface proteins translated from distinct initiation codons while sharing a common carboxyl domain (i.e., SHBs). Consequently, LHBs contains an extra N-terminal PreS domain, which is further divided into the amino-PreS1 and carboxyl-PreS2 domains. MHBs contains the PreS2 domain but lacks the PreS1 domain. LHBs is associated mainly with infectious virions but can also be found in smaller amounts on rod-shaped subviral particles. On the other hand, the spherical subviral particles are composed mainly of SHBs. LHBs plays a pivotal role in the infection and budding stages of the HBV life cycle. LHBs proteins in the virion envelope exhibit mixed topologies, with their PreS domains protruding either inwardly or outwardly (32,35

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“…The uptake of apoE-containing particles is mediated by HL [17], and in mice most plasma apoE is associated with HDL particles [17,18]. Other pathways in the modulation of plasma HDL levels are: cholesterol ester transfer protein (CETP)-mediated transfer of HDL cholesteryl esters to apoB-containing particles [19]; changes in the size and composition of HDL particles by the action of lechithin cholesterol acetyl transferase (LCAT) [20]; and uptake of whole HDL particles by a newly discovered HDL receptor, intrinsic factor vitamin B-12 receptor, also known as cubulin [21].…”

mentioning

confidence: 99%

Dietary cholic acid lowers plasma levels of mouse and human apolipoprotein A-I primarily via a transcriptional mechanism

Srivastava

Averna

2000

Eur J Biochem

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To induce dietary atherosclerosis in mice, high-fat/high-cholesterol (HF) diets are frequently supplemented with cholic acid (CA). This diet produces low plasma levels of high-density lipoprotein (HDL) and high levels of lowdensity lipoprotein (LDL). However, HF diets without any added CA, which more closely resemble human diets, increase levels of both HDL and LDL, suggesting that CA may be responsible for the lowering of HDL. Our aim was to examine the potential mechanism responsible for the lowering of HDL. Nontransgenic (NTg) C57BL mice and apoA-I-transgenic (apoAI-Tg) mice, with greatly increased basal apoA-I and HDL levels, were used. Mice were fed the following four diets: control (C), high-fat/high-cholesterol (HF), control and 1% cholate (CA) and HF 1 CA. Dietary CA reduced plasma HDL levels by 35% in NTg and 250% in apoAI-Tg mice, independent of the fat or cholesterol content of the diet. Hepatic apoA-I mRNA decreased 30% in NTg and 180% in apoAI-Tg mice. Hepatic apoA-I synthesis and apoA-I mRNA transcription rates also decreased in parallel with apoA-I mRNA levels, suggesting that the CA-induced decreases in plasma apoA-I levels occurred primarily via decreasing apoA-I mRNA transcription rates. An HF diet increased HDL levels 1.8-fold in NTg and 1.5-fold in apoAI-Tg mice. Addition of CA to the HF diet lowered HDL levels by 1.6-fold in NTg and 2.5-fold in apoAI-Tg mice. Transfection studies with the apoA-I promoter suggested the presence of a putative cis-acting element responsible for the CA-mediated down-regulation of the apoA-I promoter activity. Measurements of apoA-I regulatory protein-1 (ARP-1) mRNA, a negative regulator of the apoA-I gene in the mouse liver showed that CA increased the ARP-1 mRNA levels. Because apoA-I gene transcription alone was not sufficient to account for the lowering of plasma HDL levels, scavenger receptor-B1 (SR-B1) and hepatic lipase (HL) mRNAs levels were quantitated. The levels of SR-B1 and HL mRNA were not changed by dietary CA. These studies suggest that dietary cholate regulates plasma levels of apoA-I primarily by a transcriptional mechanism via a putative bile acid response element involving a negative regulator of apoA-I, and partly by an unidentified post-transcriptional mechanism.

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The role of lipoprotein lipase and apoprotein E in the recognition of chylomicrons and chylomicron remnants by cultured isolated mouse hepatocytes

Cited by 17 publications

References 34 publications

Low-Cholesterol and High-Fat Diets Reduce Atherosclerotic Lesion Development in ApoE-Knockout Mice

Low-Cholesterol and High-Fat Diets Reduce Atherosclerotic Lesion Development in ApoE-Knockout Mice

Identification and Characterization of Peptides That Interact with Hepatitis B Virus via the Putative Receptor Binding Site

Dietary cholic acid lowers plasma levels of mouse and human apolipoprotein A-I primarily via a transcriptional mechanism

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