SR-BI inhibits ABCG1-stimulated net cholesterol efflux from cells to plasma HDL.
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SR-BI inhibits ABCG1-stimulated net cholesterol efflux from cells to plasma HDL. / Yvan-Charvet, Laurent; Pagler, Tamara A; Wang, Nan; Senokuchi, Takafumi; Brundert, May; Li, Hongna; Rinninger, Franz; Tall, Alan R.
In: J LIPID RES, Vol. 49, No. 1, 1, 2008, p. 107-114.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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T1 - SR-BI inhibits ABCG1-stimulated net cholesterol efflux from cells to plasma HDL.
AU - Yvan-Charvet, Laurent
AU - Pagler, Tamara A
AU - Wang, Nan
AU - Senokuchi, Takafumi
AU - Brundert, May
AU - Li, Hongna
AU - Rinninger, Franz
AU - Tall, Alan R
PY - 2008
Y1 - 2008
N2 - This study compares the roles of ABCG1 and scavenger receptor class B type I (SR-BI) singly or together in promoting net cellular cholesterol efflux to plasma HDL containing active LCAT. In transfected cells, SR-BI promoted free cholesterol efflux to HDL, but this was offset by an increased uptake of HDL cholesteryl ester (CE) into cells, resulting in no net efflux. Coexpression of SR-BI with ABCG1 inhibited the ABCG1-mediated net cholesterol efflux to HDL, apparently by promoting the reuptake of CE from medium. However, ABCG1-mediated cholesterol efflux was not altered in cholesterol-loaded, SR-BI-deficient (SR-BI(-/-)) macrophages. Briefly cultured macrophages collected from SR-BI(-/-) mice loaded with acetylated LDL in the peritoneal cavity did exhibit reduced efflux to HDL. However, this was attributable to reduced expression of ABCG1 and ABCA1, likely reflecting increased macrophage cholesterol efflux to apolipoprotein E-enriched HDL during loading in SR-BI(-/-) mice. In conclusion, cellular SR-BI does not promote net cholesterol efflux from cells to plasma HDL containing active LCAT as a result of the reuptake of HDL-CE into cells. Previous findings of increased atherosclerosis in mice transplanted with SR-BI(-/-) bone marrow probably cannot be explained by a defect in macrophage cholesterol efflux.
AB - This study compares the roles of ABCG1 and scavenger receptor class B type I (SR-BI) singly or together in promoting net cellular cholesterol efflux to plasma HDL containing active LCAT. In transfected cells, SR-BI promoted free cholesterol efflux to HDL, but this was offset by an increased uptake of HDL cholesteryl ester (CE) into cells, resulting in no net efflux. Coexpression of SR-BI with ABCG1 inhibited the ABCG1-mediated net cholesterol efflux to HDL, apparently by promoting the reuptake of CE from medium. However, ABCG1-mediated cholesterol efflux was not altered in cholesterol-loaded, SR-BI-deficient (SR-BI(-/-)) macrophages. Briefly cultured macrophages collected from SR-BI(-/-) mice loaded with acetylated LDL in the peritoneal cavity did exhibit reduced efflux to HDL. However, this was attributable to reduced expression of ABCG1 and ABCA1, likely reflecting increased macrophage cholesterol efflux to apolipoprotein E-enriched HDL during loading in SR-BI(-/-) mice. In conclusion, cellular SR-BI does not promote net cholesterol efflux from cells to plasma HDL containing active LCAT as a result of the reuptake of HDL-CE into cells. Previous findings of increased atherosclerosis in mice transplanted with SR-BI(-/-) bone marrow probably cannot be explained by a defect in macrophage cholesterol efflux.
M3 - SCORING: Zeitschriftenaufsatz
VL - 49
SP - 107
EP - 114
JO - J LIPID RES
JF - J LIPID RES
SN - 0022-2275
IS - 1
M1 - 1
ER -
