Research ExplorerPublicationsSelective uptake of HDL cholesteryl esters and cholesterol e...

Selective uptake of HDL cholesteryl esters and cholesterol efflux from mouse peritoneal macrophages independent of SR-BI.

Standard

Selective uptake of HDL cholesteryl esters and cholesterol efflux from mouse peritoneal macrophages independent of SR-BI. / Brundert, May; Heeren, Joerg; Bahar-Bayansar, Mukaddes; Ewert, Anne; Moore, Kathryn J; Rinninger, Franz.

In: J LIPID RES, Vol. 47, No. 11, 11, 2006, p. 2408-2421.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Brundert, M, Heeren, J, Bahar-Bayansar, M, Ewert, A, Moore, KJ & Rinninger, F 2006, 'Selective uptake of HDL cholesteryl esters and cholesterol efflux from mouse peritoneal macrophages independent of SR-BI.', J LIPID RES, vol. 47, no. 11, 11, pp. 2408-2421. <http://www.ncbi.nlm.nih.gov/pubmed/16926440?dopt=Citation>

APA

Brundert, M., Heeren, J., Bahar-Bayansar, M., Ewert, A., Moore, K. J., & Rinninger, F. (2006). Selective uptake of HDL cholesteryl esters and cholesterol efflux from mouse peritoneal macrophages independent of SR-BI. J LIPID RES, 47(11), 2408-2421. [11]. http://www.ncbi.nlm.nih.gov/pubmed/16926440?dopt=Citation

Vancouver

Brundert M, Heeren J, Bahar-Bayansar M, Ewert A, Moore KJ, Rinninger F. Selective uptake of HDL cholesteryl esters and cholesterol efflux from mouse peritoneal macrophages independent of SR-BI. J LIPID RES. 2006;47(11):2408-2421. 11.

Bibtex

@article{bbb64847a3074a2f8f181fb494a88b97,
title = "Selective uptake of HDL cholesteryl esters and cholesterol efflux from mouse peritoneal macrophages independent of SR-BI.",
abstract = "Scavenger receptor class B type I (SR-BI) mediates the selective uptake of HDL cholesteryl esters (CEs) and facilitates the efflux of unesterified cholesterol. SR-BI expression in macrophages presumably plays a role in atherosclerosis. The role of SR-BI for selective CE uptake and cholesterol efflux in macrophages was explored. Macrophages and HDL originated from wild-type (WT) or SR-BI knockout (KO; homozygous) mice. For uptake, macrophages were incubated in medium containing 125I-/3H-labeled HDL. For lipid removal, [3H]cholesterol efflux was analyzed using HDL as acceptor. Selective uptake of HDL CE ([3H]cholesteryl oleyl ether - 125I-tyramine cellobiose) was similar in WT and SR-BI KO macrophages. Radiolabeled SR-BI KO-HDL yielded a lower rate of selective uptake compared with WT-HDL in WT and SR-BI KO macrophages. Cholesterol efflux was similar in WT and SR-BI KO cells using HDL as acceptor. SR-BI KO-HDL more efficiently promoted cholesterol removal compared with WT-HDL from both types of macrophages. Macrophages selectively take up HDL CE independently of SR-BI. Additionally, in macrophages, there is substantial cholesterol efflux that is not mediated by SR-BI. Therefore, SR-BI-independent mechanisms mediate selective CE uptake and cholesterol removal. SR-BI KO-HDL is an inferior donor for selective CE uptake compared with WT-HDL, whereas SR-BI KO-HDL more efficiently promotes cholesterol efflux.",
keywords = "Animals, Humans, Mice, Mice, Knockout, Cricetinae, Homozygote, Mice, Transgenic, Dose-Response Relationship, Drug, Cholesterol/metabolism, Antigens, CD36/metabolism/*physiology, Cholesterol Esters/metabolism/*pharmacokinetics, Kidney/embryology, Lipoproteins/metabolism, Lipoproteins, HDL/metabolism/*pharmacokinetics, Macrophages/metabolism, Macrophages, Peritoneal/*metabolism, Animals, Humans, Mice, Mice, Knockout, Cricetinae, Homozygote, Mice, Transgenic, Dose-Response Relationship, Drug, Cholesterol/metabolism, Antigens, CD36/metabolism/*physiology, Cholesterol Esters/metabolism/*pharmacokinetics, Kidney/embryology, Lipoproteins/metabolism, Lipoproteins, HDL/metabolism/*pharmacokinetics, Macrophages/metabolism, Macrophages, Peritoneal/*metabolism",
author = "May Brundert and Joerg Heeren and Mukaddes Bahar-Bayansar and Anne Ewert and Moore, {Kathryn J} and Franz Rinninger",
year = "2006",
language = "English",
volume = "47",
pages = "2408--2421",
journal = "J LIPID RES",
issn = "0022-2275",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "11",

}

RIS

TY - JOUR

T1 - Selective uptake of HDL cholesteryl esters and cholesterol efflux from mouse peritoneal macrophages independent of SR-BI.

AU - Brundert, May

AU - Heeren, Joerg

AU - Bahar-Bayansar, Mukaddes

AU - Ewert, Anne

AU - Moore, Kathryn J

AU - Rinninger, Franz

PY - 2006

Y1 - 2006

N2 - Scavenger receptor class B type I (SR-BI) mediates the selective uptake of HDL cholesteryl esters (CEs) and facilitates the efflux of unesterified cholesterol. SR-BI expression in macrophages presumably plays a role in atherosclerosis. The role of SR-BI for selective CE uptake and cholesterol efflux in macrophages was explored. Macrophages and HDL originated from wild-type (WT) or SR-BI knockout (KO; homozygous) mice. For uptake, macrophages were incubated in medium containing 125I-/3H-labeled HDL. For lipid removal, [3H]cholesterol efflux was analyzed using HDL as acceptor. Selective uptake of HDL CE ([3H]cholesteryl oleyl ether - 125I-tyramine cellobiose) was similar in WT and SR-BI KO macrophages. Radiolabeled SR-BI KO-HDL yielded a lower rate of selective uptake compared with WT-HDL in WT and SR-BI KO macrophages. Cholesterol efflux was similar in WT and SR-BI KO cells using HDL as acceptor. SR-BI KO-HDL more efficiently promoted cholesterol removal compared with WT-HDL from both types of macrophages. Macrophages selectively take up HDL CE independently of SR-BI. Additionally, in macrophages, there is substantial cholesterol efflux that is not mediated by SR-BI. Therefore, SR-BI-independent mechanisms mediate selective CE uptake and cholesterol removal. SR-BI KO-HDL is an inferior donor for selective CE uptake compared with WT-HDL, whereas SR-BI KO-HDL more efficiently promotes cholesterol efflux.

AB - Scavenger receptor class B type I (SR-BI) mediates the selective uptake of HDL cholesteryl esters (CEs) and facilitates the efflux of unesterified cholesterol. SR-BI expression in macrophages presumably plays a role in atherosclerosis. The role of SR-BI for selective CE uptake and cholesterol efflux in macrophages was explored. Macrophages and HDL originated from wild-type (WT) or SR-BI knockout (KO; homozygous) mice. For uptake, macrophages were incubated in medium containing 125I-/3H-labeled HDL. For lipid removal, [3H]cholesterol efflux was analyzed using HDL as acceptor. Selective uptake of HDL CE ([3H]cholesteryl oleyl ether - 125I-tyramine cellobiose) was similar in WT and SR-BI KO macrophages. Radiolabeled SR-BI KO-HDL yielded a lower rate of selective uptake compared with WT-HDL in WT and SR-BI KO macrophages. Cholesterol efflux was similar in WT and SR-BI KO cells using HDL as acceptor. SR-BI KO-HDL more efficiently promoted cholesterol removal compared with WT-HDL from both types of macrophages. Macrophages selectively take up HDL CE independently of SR-BI. Additionally, in macrophages, there is substantial cholesterol efflux that is not mediated by SR-BI. Therefore, SR-BI-independent mechanisms mediate selective CE uptake and cholesterol removal. SR-BI KO-HDL is an inferior donor for selective CE uptake compared with WT-HDL, whereas SR-BI KO-HDL more efficiently promotes cholesterol efflux.

KW - Animals

KW - Humans

KW - Mice

KW - Mice, Knockout

KW - Cricetinae

KW - Homozygote

KW - Mice, Transgenic

KW - Dose-Response Relationship, Drug

KW - Cholesterol/metabolism

KW - Antigens, CD36/metabolism/physiology

KW - Cholesterol Esters/metabolism/pharmacokinetics

KW - Kidney/embryology

KW - Lipoproteins/metabolism

KW - Lipoproteins, HDL/metabolism/pharmacokinetics

KW - Macrophages/metabolism

KW - Macrophages, Peritoneal/metabolism

KW - Animals

KW - Humans

KW - Mice

KW - Mice, Knockout

KW - Cricetinae

KW - Homozygote

KW - Mice, Transgenic

KW - Dose-Response Relationship, Drug

KW - Cholesterol/metabolism

KW - Antigens, CD36/metabolism/physiology

KW - Cholesterol Esters/metabolism/pharmacokinetics

KW - Kidney/embryology

KW - Lipoproteins/metabolism

KW - Lipoproteins, HDL/metabolism/pharmacokinetics

KW - Macrophages/metabolism

KW - Macrophages, Peritoneal/metabolism

M3 - SCORING: Journal article

VL - 47

SP - 2408

EP - 2421

JO - J LIPID RES

JF - J LIPID RES

SN - 0022-2275

IS - 11

M1 - 11

ER -