Fig. 3.

Macrophage VLDLR deficiency reduces intracellular triglyceride accumulation and pro-inflammatory gene expression upon VLDL. a Peritoneal macrophages from WT or VLDLR KO mice were treated with VLDL-Dil (10 μg/ml) for the indicated periods. VLDL-Dil (red) was detected by fluorescence microscopy. b Quantification of accumulated VLDL-DiI fluorescence in WT and VLDLR KO macrophages during different incubation periods. c, d Intracellular triglyceride (c) and cholesterol (d) in WT or VLDLR KO macrophages with (+) or without (−) human VLDL (30 μg/ml) challenges. e Relative mRNA levels of VLDLR and pro-inflammatory genes in WT or VLDLR KO macrophages with (+) or without (−) human VLDL (30 μg/ml) challenge. Each mRNA level was normalized to cyclophilin mRNA. c–e Data represent mean ± SD. ^# P < 0.05, ^## P < 0.01 ± VLDL; *P < 0.05, **P < 0.01, ***P < 0.001, Student’s t-test. f, g Insulin-dependent glucose uptake ability (f) and insulin signaling cascades (g) were examined in 3T3-L1 adipocytes after conditioned media treatment from WT or VLDLR KO macrophages in the presence of human VLDL (30 μg/ml). FM and CM stand for fresh media and conditioned media, respectively. f, g Data represent mean ± SD. ^# P < 0.05 vs. FM, *P < 0.05, Student’s t-test