Figure 3

The MIF-CXCR4 signaling axis regulates DiI-LDL uptake into primary human monocyte-derived macrophages. (a) Relative change in DiI signal intensity compared to negative control (in percent) in macrophages treated with siRNAs against CXCR4 or CXCR7 (n = 5). (b) Representative images of DiI-LDL signal in macrophages treated with CXCR4- or control-siRNA. (c) Relative change in DiI signal intensity compared to negative control in per cent in macrophages treated with siRNAs against CXCL12 or MIF (n = 3). (d) Relative change in DiI fluorescence intensity compared to negative control (untreated cells) after stimulation with either AMD3100 (AMD) alone for 8 or 24 hours, or CXCL12 (1 μg/ml) or MIF (1 μg/ml) for 8 or 24 hours in the absence or presence of AMD (n = 3). (e) Relative change in DiI fluorescence intensity compared to negative control siRNA after treatment with CXCR4-siRNA in the absence or the presence of MIF (1 μg/ml) for 24 hours. (f) Relative change in DiI fluorescence intensity compared to negative control (untreated cells) after stimulation with MIF (1 μg/ml) in the absence or presence of pertussis toxin (250 ng/ml) for 24 hours (n = 3). P-values were calculated with unpaired, two-tailed t-test followed by a post-hoc Dunn’s multiple comparison test. ***P < 0.0001.