Selective uptake of HDL cholesteryl esters and cholesterol efflux from mouse peritoneal macrophages independent of SR-BI.
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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, Jahrgang 47, Nr. 11, 11, 2006, S. 2408-2421.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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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 -