Review Article

Intracellular and Plasma Membrane Events in Cholesterol Transport and Homeostasis

Table 2

The contribution of specific pathways in cholesterol efflux. The estimations are from the tables, texts, and graphs in the cited papers. Some values do not give a total of 100%, probably because of the rounding of the data in the tables. Efflux values are given as a percentage of total cell cholesterol and the contribution of pathways in the original studies was estimated using inhibitors of ABCA1 and SR-BI (probucol and BLT-1), if other is not mentioned.

CellsAcceptorEfflux, %Contribution of the pathway to efflux, %Reference
UninhibitedDiffusionABCA1ABCG1SR-B1

MPM2.5% HS10 – 2671 – 7871 – 7813 – 2300 – 9[68]
AcLDL-loaded MPM2.5% HS23 – 4448 - 6331 - 4233 - 447 – 274 – 10[68]
ABCA1: MPM2.5% HS119494n.a.06[68]
ABCA1: AcLDL-loaded MPM2.5% HS159670n.a.264[68]
ABCG1: MPM2.5% HS18707023n.a.7[68]
ABCG1: AcLDL-loaded MPM2.5% HS29464650n.a.4[68]
SR-B1: MPM2.5% HS117474260n.a.[68]
SR-B1: AcLDL-loaded MPM2.5% HS2840296011n.a.[68]
mBMDM, AcLDL-loaded and GW3965-stimulated2.5% MS6 – 8n.d.4 40150 [69]
AcLDL-loaded MPM2.5% HS 976n.d.18n.d.6[70]
AcLDL-loaded J7742.5% HS576n.d.14n.d.10[70]
J7742.8% apoB-depleted HS1153n.d.17n.d.30[71]
J774, stimulated by cAMP2.8% apoB-depleted HS1351n.d.39n.d.10[71]
J774, stimulated by cAMP2.8% apoB-depleted HS (b.a. )1338n.d.60n.d.6[71]
J774, stimulated by cAMP2.8% apoB-depleted HS (a.a. )1733n.d.65n.d.7[71]
J774, stimulated by cAMP2.8% apoB-depleted HS (b.a. )1239n.d.53n.d.12[71]
J774, stimulated by cAMP2.8% apoB-depleted HS (a.a. )1538n.d.57n.d.9[71]
J774, stimulated by cAMP2.8% apoB-depleted HS (b.a.)943n.d.52n.d.5[71]
J774, stimulated by cAMP2.8% apoB-depleted HS (a.a. )1336n.d.58n.d.2[71]
J774, stimulated by cAMP2.8% apoB-depleted HS (b.a.)1231n.d.56n.d.9[71]
J774, stimulated by cAMP2.8% apoB-depleted HS (a.a. )1733n.d.62n.d.10[71]

Efflux that was not inhibited by both probucol and BLT-1 (inhibitors of ABCA1 and SR-BI); it is assumed that uninhibited efflux is a sum of aqueous diffusion and ABCG1 pathways.
Cells were isolated from the knockout mouse.
The contributions of the pathways are roughly estimated by the comparison of the efflux in the cells from KO animal versus WT cells.
Serum was pooled from 15 normolipidemic individuals; cholesterol efflux for 8 hours.
Efflux for 2 hours.
Serum was pooled from 12 normolipidemic individuals; efflux for 4 hours.
2.8% apolipoprotein B -depleted serum is equivalent to 2% serum. The serum was from healthy nonsmokers; efflux for 4 hours.
Serum is from female subjects with HDL-C = 45-51.
The data are grouped for 11 females with efflux below average (b.a.) and 11 females with efflux above average (a.a.).
Serum is from female subjects with HDL-C = 69-77.
The data are grouped for 9 females with efflux below average (b.a.) and 9 females with efflux above average (a.a.).
Serum is from male subjects with HDL-C = 36-40.
The data are grouped for 7 males with efflux below average (b.a.) and 7 males with efflux above average (a.a.).
Serum is from male subjects with HDL-C = 59-66.
The data are grouped for 8 males with efflux below average (b.a.) and 8 males with efflux above average (a.a.).
Calculated by subtraction values for other pathways from 100%.
Estimated using cell that were not treated with AcLDL and GW3965 since they have higher level of SR-B1 expression.
GW3965 is LXR agonist.
n.d.: not determined; n.a.: not applicable
AcLDL: acetylated LDL; HS: human serum; mBMDM: mouse bone marrow-derived macrophage; MPM: mouse peritoneal macrophages; MS: mouse serum.