Fig. 5

Macrophage-specific Fpn1 deficiency suppresses ABC transporters by downregulating LXRα expression. Peritoneal macrophages from Apoe^−/− and Apoe^−/−Fpn1^LysM/LysM mice were collected, cultured, and treated with the iron chelator DFP or the antioxidant α-LA as indicated. a Protein levels of ABCA1, ABCG1, LXRα, CD36 and LOX1 revealed by Western blot analysis. b Protein levels of ABCA1, ABCG1, and LXRα after the macrophages were treated with DFP (50 μM) or α-LA (200 nM) for 48 h. c The relative mRNA levels of ABCA1 and ABCG1, as determined by qPCR. d Representative images of DHE staining following treatment with DFP (50 μM) or α-LA (200 nM) for 48 h. e ApoAI-mediated cholesterol efflux in Apoe^−/−Fpn1^LysM/LysM macrophages. The cholesterol-loaded macrophages were incubated with or without ApoAI (100 µg/ml) in the presence or absence of DFP (50 μM) or α-LA (200 nM) for 24 h. The results are expressed as the percentage change in the intracellular total cholesterol amount in the presence of ApoAI relative to that in ApoAI-free medium. Data are presented as the mean ± SEM; n = 4. Statistical significance was determined using Student’s t-test and one-way ANOVA followed by Tukey’s multiple comparisons test. *P < 0.05, **P < 0.01, and ***P < 0.001 Apoe^−/−Fpn1^LysM/LysM vs. Apoe^−/−; ^†P < 0.05, ^††P < 0.01 and ^†††P < 0.001 Apoe^−/−Fpn1^LysM/LysM + DFP vs. Apoe^−/−Fpn1^LysM/LysM; ^‡P < 0.05, ^‡‡P < 0.01 Apoe^−/−Fpn1^LysM/LysM + α-LA vs. Apoe^−/−Fpn1^LysM/LysM. α-LA alpha lipoic acid