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. 2010 Oct 18;120(11):3979–3995. doi: 10.1172/JCI42315

Figure 4. S1PR2 deficiency inhibits uptake of modified LDL and stimulates cholesterol efflux in BM-derived macrophages.

Figure 4

(A) Foam cell formation assay. Macrophages from S1pr2+/+Apoe–/– (left panels) and S1pr2–/–Apoe–/– (right panels) mice were exposed to oxLDL for 6 hours. Cells containing oil red O–positive fat droplets were considered foam cells. Scale bars: 20 μm. (B) Quantified data of oil red O–positive cells. *P < 0.05. (C) Uptake of Dil-labeled acetylated–LDL (ac-LDL). Macrophages from S1pr2+/+Apoe–/– (left panel) and S1pr2–/–Apoe–/– (right panel) mice were incubated with Dil-labeled ac-LDL for 4 hours. Scale bars: 20 μm. (D) Quantified data of Dil-labeled ac-LDL uptake is shown. (n = 3 each). *P < 0.05. (E) Cholesterol efflux from cholesterol-loaded macrophages. Macrophages from S1pr2+/+Apoe–/– (white bars) and S1pr2–/–Apoe–/– (black bars) mice were loaded with [3H]-labeled cholesterol. Cholesterol-loaded macrophages were incubated in the media containing either 0.2% BSA, 2% serum (FBS), or 50 μg/ml HDL as acceptor for 6 hours. The media and cells were collected for counting [3H] radioactivity (n = 3 each). *P < 0.05. Data are expressed as mean ± SEM.