The role of scavenger receptor class B type I (SR-BI) in lipid trafficking

Rhainds, David; Brissette, Louise

doi:10.1016/s1357-2725(03)00173-0

Cited by 140 publications

(112 citation statements)

References 247 publications

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“…The involvement of the scavenger receptor class B type I (SR-BI) in carotenoid uptake has been demonstrated (van Bennekum et al 2005;During and Harrison 2007). SR-BI recognizes and binds lipoproteins, both in HepG2 cells (Rhainds et al 1999) and in vivo (Van Eck et al 2008), and mediates the internalization of their lipid contents (Rhainds and Brissette 2004). AX and CX may have been incorporated into lipoproteins present in the FCS-supplemented media, thus alleviating their active transport across the cell membrane.…”

Section: Discussionmentioning

confidence: 99%

Comparison of tetrahydrofuran, fetal calf serum, and Tween 40 for the delivery of astaxanthin and canthaxanthin to HepG2 cells

et al. 2010

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The present investigation aimed to compare fetal calf serum (FCS) and Tween 40 with the commonly employed tetrahydrofuran (THF) with respect to cytotoxicity, stability of the solubilized carotenoids, and uptake and accumulation of the xanthophylls astaxanthin (AX) and canthaxanthin (CX) in cultured human liver cells (HepG2). Incubation of HepG2 cells for 24 h with THF (C1.25%) or FCS (C11.25%) with or without AX (C25 lmol/L) or CX (C25 lmol/L) did not affect cell viability. Tween 40 (0.25-1.25% in medium) reduced cell viability by 75-99%. The stabilities of AX and CX in cell-free RPMI 1640 medium for B24 h were higher when delivered with THF instead of FCS. The doseand time-dependent accumulations of AX and CX (1-10 lmol/L) in HepG2 cells were higher when carotenoids were delivered with FCS compared to THF. In conclusion, FCS and THF, but not Tween 40, were suitable solvent systems for the delivery of AX and CX to HepG2 cells. In our experiments FCS was superior with regard to the uptake and accumulation of both carotenoids.

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Section: Discussionmentioning

confidence: 99%

Comparison of tetrahydrofuran, fetal calf serum, and Tween 40 for the delivery of astaxanthin and canthaxanthin to HepG2 cells

et al. 2010

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“…The main physiological function of SR-BI is to transfer lipids between lipoproteins and cells (48), a function that is pivotal for HCVcc cell entry (23,24,47). We thus investigated the impact of the overexpression of the G420H/G424H hSR-BI mutant, which has impaired capacity to transfer lipids despite normal HDL binding capacity (49), on infectivity of HCVfrg and HCVcc subpopulations.…”

Section: Hcvfrg Entry Depends Mostly On the Lipid Transfer Activity Omentioning

confidence: 99%

Functional and Biochemical Characterization of Hepatitis C Virus (HCV) Particles Produced in a Humanized Liver Mouse Model

Calattini¹,

Fusil²,

Mancip³

et al. 2015

Journal of Biological Chemistry

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Background:We compared viral subpopulations derived from humanized liver mouse model versus cell culture. Results:In vivo and in vitro produced particles show different biophysical properties and receptor usage. Conclusion:In vivo models allow functional investigations on how lipid metabolism and hepatic environment influence HCV entry. Significance: HCV produced from humanized liver mice may better reflect the characteristics of virus from HCV-infected patients.

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“…SR-B1 is a HDL specific receptor composed of 509 amino acid residues. SR-B1, a horse hoof-like transmembrane glycoprotein, consists of 5 domains: a large extracellular, circular domain composed of 403 amino acid residues with 9 N-terminal-linked glycosylation sites and rich in cysteines, two cytoplasmic domains (amino-terminal domain and carboxy-terminal domain), and two transmembrane domains (N-terminal domain of 28 amino acid residues and C-terminal domain of 25 residues) [23] . HDL presents or accepts cholesterol while anchored to plasma membranes via its receptor, SR-B1.…”

Section: Four Trafficking Systemsmentioning

confidence: 99%

A novel model of cholesterol efflux from lipid-loaded cells

et al. 2010

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Cholesterol efflux from lipid-loaded cells is a key athero-protective event that counteracts cholesterol uptake. The imbalance between cholesterol efflux and uptake determines the prevention or development of atherosclerosis. Many proteins and factors participate in the cholesterol efflux event. However, there are currently no systematic models of reverse cholesterol transport (RCT) that include most RCT-related factors and events. On the basis of recent research findings from other and our laboratories, we propose a novel model of one center and four systems with coupling transportation and networking regulation. This model represents a common way of cholesterol efflux; however, the systems in the model consist of different proteins/factors in different cells. In this review, we evaluate the novel model in vascular smooth muscle cells (VSMCs) and macrophages, which are the most important original cells of foam cells. This novel model consists of 1) a caveolae transport center, 2) an intracellular trafficking system of the caveolin-1 complex, 3) a transmembrane transport system of the ABC-A1 complex, 4) a transmembrane transport system of the SR-B1 complex, and 5) an extracelluar trafficking system of HDL/Apo-A1. In brief, the caveolin-1 system transports cholesterol from intracellular compartments to caveolae. Subsequently, both ABC-A1 and SR-B1 complex systems transfer cholesterol from caveolae to extracellular HDL/Apo-A1. The four systems are linked by a regulatory network. This model provides a simple and concise way to understand the dynamic process of atherosclerosis.

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The role of scavenger receptor class B type I (SR-BI) in lipid trafficking

Cited by 140 publications

References 247 publications

Comparison of tetrahydrofuran, fetal calf serum, and Tween 40 for the delivery of astaxanthin and canthaxanthin to HepG2 cells

Comparison of tetrahydrofuran, fetal calf serum, and Tween 40 for the delivery of astaxanthin and canthaxanthin to HepG2 cells

Functional and Biochemical Characterization of Hepatitis C Virus (HCV) Particles Produced in a Humanized Liver Mouse Model

A novel model of cholesterol efflux from lipid-loaded cells

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