Mechanisms regulating hepatic SR-BI expression and their impact on HDL metabolism

Leiva, Andrea; Verdejo, Hugo; Benítez, María Luisa; Martínez, Álvaro; Busso, Dolores; Rigotti, Attilio

doi:10.1016/j.atherosclerosis.2011.05.036

Cited by 61 publications

(54 citation statements)

References 115 publications

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“…This is mediated by the scavenger receptor class B member 1 (SRB1, also known as SR-BI), an integral membrane protein that is highly expressed in liver and steroidogenic tissues. SRB1 facilitates the incorporation of HDLderived cholesteryl esters through a process called selective uptake (Leiva et al, 2011). This is not associated with HDL particle internalization through endosomal or lysosomal pathways, but involves the binding of HDL to SRB1 at the cell surface, followed by passive diffusion of HDL-derived cholesteryl esters into the plasma membrane.…”

Section: Intracellular Trafficking Of Cholesterolmentioning

confidence: 99%

Role of cholesterol in SNARE-mediated trafficking on intracellular membranes

Enrich

Rentero

Hierro

et al. 2015

Journal of Cell Science

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The cell surface delivery of extracellular matrix (ECM) and integrins is fundamental for cell migration in wound healing and during cancer cell metastasis. This process is not only driven by several soluble NSF attachment protein (SNAP) receptor (SNARE) proteins, which are key players in vesicle transport at the cell surface and intracellular compartments, but is also tightly modulated by cholesterol. Cholesterol-sensitive SNAREs at the cell surface are relatively well characterized, but it is less well understood how altered cholesterol levels in intracellular compartments impact on SNARE localization and function. Recent insights from structural biology, protein chemistry and cell microscopy have suggested that a subset of the SNAREs engaged in exocytic and retrograde pathways dynamically 'sense' cholesterol levels in the Golgi and endosomal membranes. Hence, the transport routes that modulate cellular cholesterol distribution appear to trigger not only a change in the location and functioning of SNAREs at the cell surface but also in endomembranes. In this Commentary, we will discuss how disrupted cholesterol transport through the Golgi and endosomal compartments ultimately controls SNARE-mediated delivery of ECM and integrins to the cell surface and, consequently, cell migration.

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Section: Intracellular Trafficking Of Cholesterolmentioning

confidence: 99%

Role of cholesterol in SNARE-mediated trafficking on intracellular membranes

Enrich

Rentero

Hierro

et al. 2015

Journal of Cell Science

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“…miR-33a/b have several targets that include the ATP binding-cassette (ABC)A1 cholesterol transport by taking up circulating HDL. Although SR-BI knockout mice have increased plasma HDL, reduced hepatic cholesterol uptake, and decreased biliary cholesterol secretion ( 79 ), there are reports demonstrating that SR-BI knockout alone is not suffi cient to induce an atherosclerotic phenotype in mice ( 80 ). It is likely that there is a compensatory ratio of free cholesterol/CEs is maintained.…”

Section: An Increase In Mir-185 Expression Level Correlates With Highmentioning

confidence: 99%

“…by guest, on May 9, 2018 www.jlr.org Downloaded from SR-BI-independent mechanism for HDL uptake ( 79 ). In vivo studies looking at how miR-185 functions to regulate SR-B1 and how this regulation affects cholesterol homeostasis are necessary to provide more insight concerning miR-185 function and reverse cholesterol transport.…”

Section: Fig 12mentioning

confidence: 99%

Identification of miR-185 as a regulator of de novo cholesterol biosynthesis and low density lipoprotein uptake

Yang¹,

Liu²,

Pellicane³

et al. 2014

Journal of Lipid Research

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“…These observations can be explained by the fact that an increased hepatic SR-BI expression promotes RCT, whereas ablation reduces RCT 24) . Several studies in rodents have focused on the regulation of SR-BI, in which fatty acids, polyunsaturated fats, cholesterol, estradiol, vitamin E, lipopolysaccharide, TNFα and IL-1 have been shown to play an important role in inducing the differential expression of the SR-B1 receptor 25) . However, few studies have been reported the role of SR-B1 in vitamin A metabolism.…”

Section: Vitamin a Regulates The Hepatic Lxrα And Rxrα Expressionmentioning

confidence: 99%

Vitamin A-enriched Diet Modulates Reverse Cholesterol Transport in Hypercholesterolemic Obese Rats of the WNIN/Ob Strain

Anamthathmakula¹,

Jeyakumar²,

Giridharan³

et al. 2014

JAT

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Aim: Vitamin A plays a major role in lipid metabolism. Previously, we reported that chronic vitamin A feeding (129 mg/kg) for two months normalized the abnormally high plasma HDL-cholesterol (HDL-C) levels in hypercholesterolemic obese rats by upregulating the hepatic scavenger receptor class B type 1 (SR-BI) expression. In this report, we hypothesize that the administration of a dose less than 129 mg of vitamin A/kg would also be effective in lowering the plasma HDL-C levels in these rats. Methods: Changes in the activity and expression of proteins related to RCT were analyzed together with blood parameters in five-month-old male lean and obese rats supplemented with 2.6 (control group), 26, 52 and 129 mg of vitamin A/kg as retinyl palmitate for 20 weeks. Results: Vitamin A supplementation in the obese rats decreased the plasma HDL-C levels with a concomitant increase in the hepatic SR-BI expression and lipase activity compared to that observed in the control diet-fed obese rats treated with 2.6 mg of vitamin A/kg diet. Furthermore, vitamin A supplementation at doses of 52 and 129 mg/kg diet reduced the plasma lecithin cholesterol acyltransferase activity and increased the hepatic ATP-binding cassette transporter protein A1 expression in the obese rats. Interestingly, most of these changes were not observed in the lean rats fed a vitamin A-enriched diet. Conclusions: Chronic feeding of a vitamin A-enriched diet in hypercholesterolemic obese rats normalizes the plasma HDL-C level and presumably improves RCT, with an effective dose of 52 mg/kg diet. Further studies should focus on the pharmacological potential of vitamin A supplementation to correct an abnormal human obesity-associated lipoprotein metabolism.

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Mechanisms regulating hepatic SR-BI expression and their impact on HDL metabolism

Cited by 61 publications

References 115 publications

Role of cholesterol in SNARE-mediated trafficking on intracellular membranes

Role of cholesterol in SNARE-mediated trafficking on intracellular membranes

Identification of miR-185 as a regulator of de novo cholesterol biosynthesis and low density lipoprotein uptake

Vitamin A-enriched Diet Modulates Reverse Cholesterol Transport in Hypercholesterolemic Obese Rats of the WNIN/Ob Strain

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