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$Probucol inhibits cholesterol efflux differently in NF cells vs F cells. The effect of a fixed probucol dose on apoA-I cholesterol efflux capacity in THP-1 non-foam (A) and foam cells (B). THP-1 cells were radiolabeled with [3H]cholesterol (48 h) or [3H]cholesterol, AcLDL (50 µg/ml) and 1% FBS. Cells were incubated for 48 h and treated with 10 µM 9cRA and 5 µg/ml 22-OH for 18 h as indicated in “Methods.” Cholesterol efflux was then initiated by the addition of apoA-I at the indicated doses for 4 h. The fractional cholesterol efflux is plotted as a function of acceptor concentration. In all experiments, efflux of [3H]cholesterol is expressed as mean±SD of triplicate measurements and represents three experiments. C. Concentration-dependent effect of probucol on apoA-I-mediated cholesterol efflux in THP-1 and <t>J774</t> non foam cells respectively. Monolayers were radio labeled for 48 h as described in “Methods.” THP-1 and J774 cells were then equilibrated with 0.2% BSA and incubated with 10 µM 9cRA and 5 µg/ml 22-OH or cAMP (0.3 mM) for 18 h respectively. Monolayers were then incubated in the presence of increasing concentrations of probucol for 2h. After probucol treatment, cells were washed and incubated with RPMI containing 25 µg/ml lipid-free apoA-I for 4 h. Data are from a representative experiment with triplicate wells (n=3). Values are expressed as means + S.D. D. Efflux to apoA-I in the presence of probucol is almost abolished, in the BHK expressing ABCA1 cell type. BHK cells were grown as described in “Methods.” ABCA1-expressing BHK cells were radio labeled with [3H]cholesterol for 48 h in 1% FCS. To induce expression of ABCA1, BHK cells were incubated with 10 nM mifepristone containing 0.1% BSA for 18–20 h. Cell were treated with probucol for 2 h, washed and incubated with apoA-I for 24 h. Insert represents specific cholesterol efflux after subtracting efflux to BSA (0.2%) including diffusion. Results shown are representative of three independent experiments.$
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1) Product Images from "Probucol treatment is associated with an ABCA1-independent mechanism of cholesterol efflux to lipid poor apolipoproteins from foam cell macrophages"

Article Title: Probucol treatment is associated with an ABCA1-independent mechanism of cholesterol efflux to lipid poor apolipoproteins from foam cell macrophages

Journal: BBA Advances

doi: 10.1016/j.bbadva.2021.100003

$Probucol inhibits cholesterol efflux differently in NF cells vs F cells. The effect of a fixed probucol dose on apoA-I cholesterol efflux capacity in THP-1 non-foam (A) and foam cells (B). THP-1 cells were radiolabeled with [3H]cholesterol (48 h) or [3H]cholesterol, AcLDL (50 µg/ml) and 1% FBS. Cells were incubated for 48 h and treated with 10 µM 9cRA and 5 µg/ml 22-OH for 18 h as indicated in “Methods.” Cholesterol efflux was then initiated by the addition of apoA-I at the indicated doses for 4 h. The fractional cholesterol efflux is plotted as a function of acceptor concentration. In all experiments, efflux of [3H]cholesterol is expressed as mean±SD of triplicate measurements and represents three experiments. C. Concentration-dependent effect of probucol on apoA-I-mediated cholesterol efflux in THP-1 and J774 non foam cells respectively. Monolayers were radio labeled for 48 h as described in “Methods.” THP-1 and J774 cells were then equilibrated with 0.2% BSA and incubated with 10 µM 9cRA and 5 µg/ml 22-OH or cAMP (0.3 mM) for 18 h respectively. Monolayers were then incubated in the presence of increasing concentrations of probucol for 2h. After probucol treatment, cells were washed and incubated with RPMI containing 25 µg/ml lipid-free apoA-I for 4 h. Data are from a representative experiment with triplicate wells (n=3). Values are expressed as means + S.D. D. Efflux to apoA-I in the presence of probucol is almost abolished, in the BHK expressing ABCA1 cell type. BHK cells were grown as described in “Methods.” ABCA1-expressing BHK cells were radio labeled with [3H]cholesterol for 48 h in 1% FCS. To induce expression of ABCA1, BHK cells were incubated with 10 nM mifepristone containing 0.1% BSA for 18–20 h. Cell were treated with probucol for 2 h, washed and incubated with apoA-I for 24 h. Insert represents specific cholesterol efflux after subtracting efflux to BSA (0.2%) including diffusion. Results shown are representative of three independent experiments.$
Figure Legend Snippet: Probucol inhibits cholesterol efflux differently in NF cells vs F cells. The effect of a fixed probucol dose on apoA-I cholesterol efflux capacity in THP-1 non-foam (A) and foam cells (B). THP-1 cells were radiolabeled with [3H]cholesterol (48 h) or [3H]cholesterol, AcLDL (50 µg/ml) and 1% FBS. Cells were incubated for 48 h and treated with 10 µM 9cRA and 5 µg/ml 22-OH for 18 h as indicated in “Methods.” Cholesterol efflux was then initiated by the addition of apoA-I at the indicated doses for 4 h. The fractional cholesterol efflux is plotted as a function of acceptor concentration. In all experiments, efflux of [3H]cholesterol is expressed as mean±SD of triplicate measurements and represents three experiments. C. Concentration-dependent effect of probucol on apoA-I-mediated cholesterol efflux in THP-1 and J774 non foam cells respectively. Monolayers were radio labeled for 48 h as described in “Methods.” THP-1 and J774 cells were then equilibrated with 0.2% BSA and incubated with 10 µM 9cRA and 5 µg/ml 22-OH or cAMP (0.3 mM) for 18 h respectively. Monolayers were then incubated in the presence of increasing concentrations of probucol for 2h. After probucol treatment, cells were washed and incubated with RPMI containing 25 µg/ml lipid-free apoA-I for 4 h. Data are from a representative experiment with triplicate wells (n=3). Values are expressed as means + S.D. D. Efflux to apoA-I in the presence of probucol is almost abolished, in the BHK expressing ABCA1 cell type. BHK cells were grown as described in “Methods.” ABCA1-expressing BHK cells were radio labeled with [3H]cholesterol for 48 h in 1% FCS. To induce expression of ABCA1, BHK cells were incubated with 10 nM mifepristone containing 0.1% BSA for 18–20 h. Cell were treated with probucol for 2 h, washed and incubated with apoA-I for 24 h. Insert represents specific cholesterol efflux after subtracting efflux to BSA (0.2%) including diffusion. Results shown are representative of three independent experiments.

Techniques Used: Incubation, Concentration Assay, Labeling, Expressing, Diffusion-based Assay

Probucol results in less efflux inhibition in foam cells than non-foam cells. (A, B, C and D) Monolayers of J774 cells (A, B) and THP-1 cells (C, D) were labeled with 2 μCi/mL [3H]cholesterol (non-foam, A, C) or [3H]cholesterol and AcLDL (foam, B, D; 50 µg/ml), for 48 h in RPMI medium 1640 with 1% FCS. Cells were then incubated for 18 h with 0.2% BSA or not in the presence (solid bars) or absence (hatched bars) of 0.3 mM cpt-cAMP followed by incubation with or without 10 μM probucol as described in “Methods.” After 2 h of probucol treatment, cells were washed and then incubated with RPMI medium 1640 containing 25 μg/ml lipid-free apoA-I for 4 h. Data are from a representative experiment with triplicate wells (n=3). Values are expressed as mean ± SD. *P < 0.05 by Student's t-test.

Figure Legend Snippet: Probucol results in less efflux inhibition in foam cells than non-foam cells. (A, B, C and D) Monolayers of J774 cells (A, B) and THP-1 cells (C, D) were labeled with 2 μCi/mL [3H]cholesterol (non-foam, A, C) or [3H]cholesterol and AcLDL (foam, B, D; 50 µg/ml), for 48 h in RPMI medium 1640 with 1% FCS. Cells were then incubated for 18 h with 0.2% BSA or not in the presence (solid bars) or absence (hatched bars) of 0.3 mM cpt-cAMP followed by incubation with or without 10 μM probucol as described in “Methods.” After 2 h of probucol treatment, cells were washed and then incubated with RPMI medium 1640 containing 25 μg/ml lipid-free apoA-I for 4 h. Data are from a representative experiment with triplicate wells (n=3). Values are expressed as mean ± SD. *P < 0.05 by Student's t-test.

Techniques Used: Inhibition, Labeling, Incubation

Figure Legend Snippet: Macrophage foam cells are less sensitive to probucol-mediated inhibition of cholesterol efflux than non-foam cells.

Techniques Used: Inhibition

The effect of probucol on cholesterol efflux in foam cells without ABCA1 expression. Probucol produces a lesser degree of efflux inhibition in non-cAMP stimulated J774 foam cells vs non-foam cells. Monolayers were labeled with 2 μCi/ml [3H]cholesterol (A) or [3H]cholesterol and AcLDL (B, 50 µg/ml), for 48 h in RPMI medium 1640 with 1% FCS. Cells were then incubated for 18 h or not with 0.2% BSA in the absence of 0.3 mM cpt-cAMP followed by incubation with 10 μM probucol for 2 h. Cells were washed and then incubated with medium containing 25 μg/ml lipid-free apoA-I for 24 h. C. Probucol completely inhibits cholesterol efflux in the absence of ABCA1 expression in non-mifepristone induced BHK cells. BHK cells were labelled with [3H]cholesterol 48 h, 1% FCS. Afterwards, cells were incubated in DMEM containing 0.2% BSA for 18–20 h. This was followed by an incubation with 10 μM probucol for 2 h. Non-induced BHK cells were washed and incubated with medium containing 10 μg/ml lipid-free apoA-I for 24 h. BHK cells incubated alone were used as control. Inset represents specific cholesterol efflux inhibited by probucol obtained after subtracted cholesterol efflux from background.D. Non-stimulated J774 and BHK cells do not express ABCA1 transporter protein. Cells were grown as described in Materials and methods, cells were lysed at 4°C with 20 mM Tris, 5 mM EDTA, and 5 mM EGTA; pH 7.5 containing 0.5% n-dodecylmaltoside. Protein concentration was determined by standard assay (Bio-Rad). Cells were separated by SDS-PAGE (4–22.5%) and immunoblotted using antibodies against human ABCA1 and the loading control glyceraldehyde 3-phosphate dehydrogenase (GAPDH). The molecular weight (Bio-Rad) is shown on the right of the gel. Data are from a representative experiment with triplicate wells (n=3). Values are expressed as mean±SD. *P < 0.05 by Student's t-test. NF; non foam, F; foam

Figure Legend Snippet: The effect of probucol on cholesterol efflux in foam cells without ABCA1 expression. Probucol produces a lesser degree of efflux inhibition in non-cAMP stimulated J774 foam cells vs non-foam cells. Monolayers were labeled with 2 μCi/ml [3H]cholesterol (A) or [3H]cholesterol and AcLDL (B, 50 µg/ml), for 48 h in RPMI medium 1640 with 1% FCS. Cells were then incubated for 18 h or not with 0.2% BSA in the absence of 0.3 mM cpt-cAMP followed by incubation with 10 μM probucol for 2 h. Cells were washed and then incubated with medium containing 25 μg/ml lipid-free apoA-I for 24 h. C. Probucol completely inhibits cholesterol efflux in the absence of ABCA1 expression in non-mifepristone induced BHK cells. BHK cells were labelled with [3H]cholesterol 48 h, 1% FCS. Afterwards, cells were incubated in DMEM containing 0.2% BSA for 18–20 h. This was followed by an incubation with 10 μM probucol for 2 h. Non-induced BHK cells were washed and incubated with medium containing 10 μg/ml lipid-free apoA-I for 24 h. BHK cells incubated alone were used as control. Inset represents specific cholesterol efflux inhibited by probucol obtained after subtracted cholesterol efflux from background.D. Non-stimulated J774 and BHK cells do not express ABCA1 transporter protein. Cells were grown as described in Materials and methods, cells were lysed at 4°C with 20 mM Tris, 5 mM EDTA, and 5 mM EGTA; pH 7.5 containing 0.5% n-dodecylmaltoside. Protein concentration was determined by standard assay (Bio-Rad). Cells were separated by SDS-PAGE (4–22.5%) and immunoblotted using antibodies against human ABCA1 and the loading control glyceraldehyde 3-phosphate dehydrogenase (GAPDH). The molecular weight (Bio-Rad) is shown on the right of the gel. Data are from a representative experiment with triplicate wells (n=3). Values are expressed as mean±SD. *P < 0.05 by Student's t-test. NF; non foam, F; foam

Techniques Used: Expressing, Inhibition, Labeling, Incubation, Control, Protein Concentration, SDS Page, Molecular Weight

Figure Legend Snippet: Probucol inhibits cholesterol efflux in J774 macrophages non-expressing ABCA1.

Techniques Used: Inhibition

Probucol does not alter ABCA1 nor ABCG1 protein expression in foam cells and non-foam cells. Cells were treated as described above, and after probucol incubation they were washed with PBS and solubilized and separated by (4-22.5%) SDS-PAGE. (A, D) ABCA1 from J774 and THP-1 cells lysis was detected by anti-ABCA1 antibody respectively. (B, C, and D) Changes in ABCA1 protein expression were determined by normalizing against the densitometric intensity of GAPDH. (E) Human ABCG1-overexpressing CHO-K1 cells were labeled with 1 µCi/ml [3H]cholesterol for 24 h, washed, and then equilibrated for 2 h in the presence of absence of different concentration of probucol. Efflux was promoted for 6 h to 12.5 µg/ml of HDL. (F) Probucol treatment did not significantly affect ABCG1 protein expression in THP-1 foam cells. ABCG1 from THP-1 cells lysis was detected by anti-ABCG1 antibody. Changes in ABCA1 protein expression were determined by normalizing against the densitometric intensity of GAPDH. Each sample was run in triplicate. Values are expressed as means ± SD. GAPDH was used as a loading control. *P < 0.05 by Student's t-test.

Figure Legend Snippet: Probucol does not alter ABCA1 nor ABCG1 protein expression in foam cells and non-foam cells. Cells were treated as described above, and after probucol incubation they were washed with PBS and solubilized and separated by (4-22.5%) SDS-PAGE. (A, D) ABCA1 from J774 and THP-1 cells lysis was detected by anti-ABCA1 antibody respectively. (B, C, and D) Changes in ABCA1 protein expression were determined by normalizing against the densitometric intensity of GAPDH. (E) Human ABCG1-overexpressing CHO-K1 cells were labeled with 1 µCi/ml [3H]cholesterol for 24 h, washed, and then equilibrated for 2 h in the presence of absence of different concentration of probucol. Efflux was promoted for 6 h to 12.5 µg/ml of HDL. (F) Probucol treatment did not significantly affect ABCG1 protein expression in THP-1 foam cells. ABCG1 from THP-1 cells lysis was detected by anti-ABCG1 antibody. Changes in ABCA1 protein expression were determined by normalizing against the densitometric intensity of GAPDH. Each sample was run in triplicate. Values are expressed as means ± SD. GAPDH was used as a loading control. *P < 0.05 by Student's t-test.

Techniques Used: Expressing, Incubation, SDS Page, Lysis, Labeling, Concentration Assay, Control

Characterization of lipidated apoA-I-containing particles generated from pretreated THP-1 cells with probucol. Monolayers were labeled with 2 μCi/ml [3H]cholesterol for 48 h in RPMI medium 1640 with 1% FCS. After 2 h of probucol treatment, cells were washed and then incubated with RPMI medium 1640 containing 10 μg/ml lipid-free apoA-I for 24 h. Afterwards, the media were collected and prepared as described in “Experimental Procedures.” Samples were separated by 2D-PAGGE and apoA-I was detected by anti-apoA-I antibody as described in “Methods.” (A, B): J774 non-foam and foam cells whole medium. (C, D): Human THP-1 macrophage non foam and foam cells whole medium. Molecular size markers (diameter in nm) are indicated. The HDL particle diameters are derived from the relative mobility values of the centers of the various bands. Molecular weight markers were revealed by Ponceau S. (E, F). Nascent HDL (nHDL) particles formed from foam cells pretreated with probucol contain more lipids than those from non foam cells. radioactivity applied to gel electrophoresis. Radioactivity appearing in gels corresponding to apoA-I and apoA-I + probucol was counted as described in “Methods.” [3H]cholesterol (E) from foam cells versus (F) non foam cells in the presence of apoA-I or apoA-I + probucol was expressed as a percentage of control (100%, in the absence of apoA-I). Results shown are representative of three independent experiments. *P < 0.05 by Student's t-test.

Figure Legend Snippet: Characterization of lipidated apoA-I-containing particles generated from pretreated THP-1 cells with probucol. Monolayers were labeled with 2 μCi/ml [3H]cholesterol for 48 h in RPMI medium 1640 with 1% FCS. After 2 h of probucol treatment, cells were washed and then incubated with RPMI medium 1640 containing 10 μg/ml lipid-free apoA-I for 24 h. Afterwards, the media were collected and prepared as described in “Experimental Procedures.” Samples were separated by 2D-PAGGE and apoA-I was detected by anti-apoA-I antibody as described in “Methods.” (A, B): J774 non-foam and foam cells whole medium. (C, D): Human THP-1 macrophage non foam and foam cells whole medium. Molecular size markers (diameter in nm) are indicated. The HDL particle diameters are derived from the relative mobility values of the centers of the various bands. Molecular weight markers were revealed by Ponceau S. (E, F). Nascent HDL (nHDL) particles formed from foam cells pretreated with probucol contain more lipids than those from non foam cells. radioactivity applied to gel electrophoresis. Radioactivity appearing in gels corresponding to apoA-I and apoA-I + probucol was counted as described in “Methods.” [3H]cholesterol (E) from foam cells versus (F) non foam cells in the presence of apoA-I or apoA-I + probucol was expressed as a percentage of control (100%, in the absence of apoA-I). Results shown are representative of three independent experiments. *P < 0.05 by Student's t-test.

Techniques Used: Generated, Labeling, Incubation, Derivative Assay, Molecular Weight, Radioactivity, Nucleic Acid Electrophoresis, Control

$Dynamics of nascent HDL generated from foam cells in the presence of probucol. Radiolabelled [3H]cholesterol loaded nascent HDL (nHDL)-like lipoprotein apoA-I derived from THP-1 foam cells pretreated with or without probucol were incubated with normolipidemic human plasma for 6 h at 37°C. After incubation, apoB was precipitated with 50/50 vol/vol 20% PEG 6000. Apo B containing particle fractions were dialyzed and [3H]cholesterol transfer was calculated between nHDL and apo B fractions as indicated (A). Counts were made in triplicates. B. Probucol effect on free cholesterol oxidation by cholesterol oxidase in J774 mouse macrophages (C) and in THP-1 non-foam and foam macrophages. Monolayers were labeled with 3 μCi/ml [3H]cholesterol for 48 h with 1% FCS or with 3 μCi/ml [3H]cholesterol, AcLDL (50 µg/ml) and 1% FCS for 48 h with 1% FCS. Cells were treated with probucol as described above, but the incubation with cAMP was done with 10 μM 9cRA and 5 μg/ml 22-OH. Data are from a representative experiment with triplicate wells (n=3). Values are expressed as mean±SD. *P < 0.05 by Student's t-test. Control cells (CTR) shows the results from non-treated cells, while CTR-probucol (PB) shows the results from cells treated with probucol 10 mM for 2h.$
Figure Legend Snippet: Dynamics of nascent HDL generated from foam cells in the presence of probucol. Radiolabelled [3H]cholesterol loaded nascent HDL (nHDL)-like lipoprotein apoA-I derived from THP-1 foam cells pretreated with or without probucol were incubated with normolipidemic human plasma for 6 h at 37°C. After incubation, apoB was precipitated with 50/50 vol/vol 20% PEG 6000. Apo B containing particle fractions were dialyzed and [3H]cholesterol transfer was calculated between nHDL and apo B fractions as indicated (A). Counts were made in triplicates. B. Probucol effect on free cholesterol oxidation by cholesterol oxidase in J774 mouse macrophages (C) and in THP-1 non-foam and foam macrophages. Monolayers were labeled with 3 μCi/ml [3H]cholesterol for 48 h with 1% FCS or with 3 μCi/ml [3H]cholesterol, AcLDL (50 µg/ml) and 1% FCS for 48 h with 1% FCS. Cells were treated with probucol as described above, but the incubation with cAMP was done with 10 μM 9cRA and 5 μg/ml 22-OH. Data are from a representative experiment with triplicate wells (n=3). Values are expressed as mean±SD. *P < 0.05 by Student's t-test. Control cells (CTR) shows the results from non-treated cells, while CTR-probucol (PB) shows the results from cells treated with probucol 10 mM for 2h.

Techniques Used: Generated, Derivative Assay, Incubation, Clinical Proteomics, Labeling, Control

Macrophage foam cells are more sensitive to probucol-mediated decrease of the total accessible plasma membrane pool of cholesterol than non-foam cells.

Figure Legend Snippet: Macrophage foam cells are more sensitive to probucol-mediated decrease of the total accessible plasma membrane pool of cholesterol than non-foam cells.

Techniques Used: Clinical Proteomics, Membrane, Inhibition

Figure Legend Snippet: Summary of main findings.

Techniques Used: Expressing, Functional Assay, Generated, Transferring

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