Infliximab Reverses Suppression of Cholesterol Efflux Proteins by TNF-α: A Possible Mechanism for Modulation of Atherogenesis
Figure 5
Infliximab nullifies augmented oxLDL uptake and accumulation in THP-1 macrophages induced by TNF-. (a) THP-1 differentiated macrophages were incubated with 50 μg/mL oxLDL for 18 h, followed by an additional 3 h in the presence of 5 μg/mL Dil-oxLDL and RPMI alone (Control), TNF- (100 U/mL), TNF- (100 U/mL) + infliximab (5 g/mL), and infliximab (5 g/mL). Dil-oxLDL accumulation was measured by fluorescent intensity with a Nikon A1 microscopy unit with 40x magnification and photographed with a DS-Ri1 digital camera. Fluorescent intensity was quantified from at least 3 random fields ( pixels) per slide, from 3 slides per experimental condition, and graphed. (b) THP-1 differentiated macrophages were incubated with 50 μg/mL oxLDL for 18 h, followed by an additional 18 h under the conditions detailed in part (a) above. Foam cell formation (FCF) was calculated as a percentage of Oil-Red-O stained cells. All results are presented as a percent of control cells with control set at 100% and expressed as mean ± SEM of five independent experiments. **; *** versus control cells; #; ## versus TNF- treated cells.
