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1.
FIGURE 3

FIGURE 3. Atherogenic lipids downregulate ADAM10 surface expression on CXCL16+ cells. From: Atherogenic Lipids Induce HDL Uptake and Cholesterol Efflux in Human Macrophages by Upregulating Transmembrane Chemokine CXCL16, without Engaging CXCL16-dependent Cell Adhesion.

Mo were cultured with or without the indicated stimuli. Summary data are shown for the percent of CXCL16+ADAM10+ cells as a function of cell stimulus. Data are from 3 independent experiments using 3 different donors and are presented as the mean ± SEM.

Jana Barlic, et al. J Immunol. ;182(12):7928-7936.
2.
FIGURE 2

FIGURE 2. Oxidized lipids inhibit release of the CXCL16 chemokine domain from monocytes. From: Atherogenic Lipids Induce HDL Uptake and Cholesterol Efflux in Human Macrophages by Upregulating Transmembrane Chemokine CXCL16, without Engaging CXCL16-dependent Cell Adhesion.

Mo were cultured with or without the stimuli listed on the x-axis (concentrations as in Figure 1). Cell culture supernatants were collected at indicated time points and analyzed for the presence of CXCL16 by enzyme-linked immunosorbent assay (ELISA). Data represent the mean ± SEM from 3 independent experiments using 3 different donors with each condition tested in triplicate.

Jana Barlic, et al. J Immunol. ;182(12):7928-7936.
3.
FIGURE 1

FIGURE 1. OxLDL and oxidized linoleic acid components of LDL specifically promote CXCL16 up-regulation on human blood monocyte-derived Mϕ. From: Atherogenic Lipids Induce HDL Uptake and Cholesterol Efflux in Human Macrophages by Upregulating Transmembrane Chemokine CXCL16, without Engaging CXCL16-dependent Cell Adhesion.

Mo were isolated, cultured and stimulated as described in Materials and Methods. A–C, Summary data of the percent of total cells with the indicated immunophenotype as a function of cell stimulus and incubation time. Donors were the same in A through C. Data are from 4 independent experiments using 8 different donors and are presented as the mean ± SEM.

Jana Barlic, et al. J Immunol. ;182(12):7928-7936.
4.
FIGURE 9

FIGURE 9. Silencing of endogenous CXCL16 decreases production of macrophage ApoE. From: Atherogenic Lipids Induce HDL Uptake and Cholesterol Efflux in Human Macrophages by Upregulating Transmembrane Chemokine CXCL16, without Engaging CXCL16-dependent Cell Adhesion.

Mo were transfected with sRNAi listed on the x-axis and then cultured for 6, 12 or 24 h with or without 50 µg/ml oxLDL. Cell culture supernatants were collected at indicated time points and analyzed for the presence of panApoE by ELISA. Data represent the mean ± SEM from 3 different donors with each condition tested in triplicate.*p < 0.05 vs the corresponding negative control sRNAi (-Cmed) value for the same time point.

Jana Barlic, et al. J Immunol. ;182(12):7928-7936.
5.
FIGURE 6

FIGURE 6. CXCL16 promotes HDL uptake in Mϕ. From: Atherogenic Lipids Induce HDL Uptake and Cholesterol Efflux in Human Macrophages by Upregulating Transmembrane Chemokine CXCL16, without Engaging CXCL16-dependent Cell Adhesion.

Uptake of Dil-HDL was performed as described in Materials and Methods. Cell-associated fluorescence was expressed as nanograms of Dil-HDL per milligram of total cellular protein. A, Mϕ, which were differentiated in presence of 50 µg/ml oxLDL for 24 h, were incubated with 4 µg/ml rat IgG2a or CXCL16 mAb before Dil-HDL internalization assay. B, Mo were nucleofected with 150 nM of CXCL16-specific (CXCL16) or negative control (-Cmed) sRNAi and then cultured for 24 h with or without 50 µg/ml oxLDL, 10 µg/ml 9-HODE or 10 µg/ml 13-HODE. Data represent the mean ± SEM from 4 donors. *p < 0.05 and **p < 0.01 vs the corresponding unblocked control value in A.
*p < 0.05 for the indicated values vs the corresponding lipid-stimulated negative control sRNAi (-Cmed) value in B.

Jana Barlic, et al. J Immunol. ;182(12):7928-7936.
6.
FIGURE 5

FIGURE 5. CXCL16 promotes oxLDL internalization in Mϕ. From: Atherogenic Lipids Induce HDL Uptake and Cholesterol Efflux in Human Macrophages by Upregulating Transmembrane Chemokine CXCL16, without Engaging CXCL16-dependent Cell Adhesion.

Uptake of Dil-oxLDL was performed as detailed in Materials and Methods. Cell-associated fluorescence was expressed as nanograms of Dil-oxLDL per milligram of total cellular protein. A, Prior to Dil-oxLDL internalization assay, Mϕ were incubated for 45 min at 37°C with 4 µg/ml of isotype control or mAbs recognizing CD36, SR-A, CXCL16 or CD68. B, Mo were nucleofected with 150 nM of the indicated CXCL16-specific (CXCL16) or negative control (-Cmed) sRNAi and then cultured for 24 h with or without 50 µg/ml oxLDL, 10 µg/ml 9-HODE or 10 µg/ml 13-HODE. Values shown are the mean (±SEM) of n=4 donors for each condition.

Jana Barlic, et al. J Immunol. ;182(12):7928-7936.
7.
FIGURE 8

FIGURE 8. CXCL16-dependent uptake of oxLDL affects expression of atheroprotective genes. From: Atherogenic Lipids Induce HDL Uptake and Cholesterol Efflux in Human Macrophages by Upregulating Transmembrane Chemokine CXCL16, without Engaging CXCL16-dependent Cell Adhesion.

Mo were nucleofected with 150 nM of CXCL16-specific (CXCL16) or negative control (-Cmed) sRNAi and then cultured for 12, 24 or 48 h with or without 50 µg/ml oxLDL. Cells were harvested at indicated times, RNA isolated as described in Materials and Methods, and accumulation of mRNA for ABCA1 (A), ABCG1(B) and ApoE(C) was examined. Results represent the mean ± SEM and are from 5 independent experiments with each condition tested in triplicate. Donors were the same in A–C. *p < 0.05 and **p < 0.01 vs the corresponding negative control sRNAi (-Cmed) value for the same time point.

Jana Barlic, et al. J Immunol. ;182(12):7928-7936.
8.
FIGURE 7

FIGURE 7. CXCL16 expression increases 3H-Cholesterol release from Mϕ. From: Atherogenic Lipids Induce HDL Uptake and Cholesterol Efflux in Human Macrophages by Upregulating Transmembrane Chemokine CXCL16, without Engaging CXCL16-dependent Cell Adhesion.

Mo were nucleofected with 150 nM of CXCL16-specific (CXCL16) or negative control (-Cmed) sRNAi and then cultured for 24 h with 50 µg/ml acLDL in the presence of radioactive cholesterol. Cells were equilibrated, washed and efflux was stimulated by incubating Mϕ in media containing lipid-poor acceptors for 6, 12 or 24 h. A, Macrophage 3H-Cholesterol efflux to human HDL. B, The release of 3H-Cholesterol to purified human ApoA-1. Results represent the mean ± SEM and are from 3 independent experiments using 3 different donors with each condition tested in triplicate. *p < 0.05, comparing the indicated value to the corresponding negative control sRNAi (-Cmed) value for the same time point.

Jana Barlic, et al. J Immunol. ;182(12):7928-7936.
9.
FIGURE 4

FIGURE 4. CXCL16-CXCR6 axis does not promote adhesion of Mϕ to coronary artery smooth muscle cells (CASMCs). From: Atherogenic Lipids Induce HDL Uptake and Cholesterol Efflux in Human Macrophages by Upregulating Transmembrane Chemokine CXCL16, without Engaging CXCL16-dependent Cell Adhesion.

Static adhesion of Mϕ to CASMCs, which were cultured with 25 µg/ml oxLDL for 24 h. The adhesion assay was performed as described in Materials and Methods. A, Prior to the adhesion assay, Mo or Mϕ were blocked for 45 min at 37°C with the following agents: 5 µg/ml isotype control rat IgG2b or CX3CR1 mAb or 4 µg/ml rat IgG2a or CXCL16 mAb. B, Mo were nucleofected with 150 nM of the indicated CXCL16-specific (CXCL16) or negative control (-Cmed) sRNAi and then cultured for 24 h in the presence or absence of atherogenic lipids. Data in A are from 3 independent experiments using Mo from 3 different donors with each condition tested in duplicate. Results in B are from 4 independent experiments using 4 different donors, each condition tested in triplicate. Data are expressed as the mean ± SEM.

Jana Barlic, et al. J Immunol. ;182(12):7928-7936.

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