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. 2017 Nov 22;8:1700. doi: 10.1038/s41467-017-01711-0

Fig. 7.

Fig. 7

MafB critically regulates C1q-dependent gene expression. a Activation of the C1q promoters by MafB or the PPARδ and RXRα complex was compared using a luciferase assay. The data are from one experiment that was representative of two independent experiments. b Empty vector (mock), MafB, c-Maf, PPARδ/RXRα, PPARγ/RXRα, LXRα/RXRα, or RXRα-expressing vectors were transfected into RAW264.7 cells. The expression of Mafb, C1qa, C1qb, and C1qc was analyzed using qRT-PCR (n = 3 for each group). The data are from one experiment that was representative of at least two independent experiments. c Control macrophages were treated with GW0742/9cRA (PPARδ/RXRα agonist), T1317/9cRA (LXRα/RXRα agonist), ATRA (RAR agonist), dexamethasone (glucocorticoid), and INFγ. Mafb expression was analyzed using qRT-PCR (n = 3 for the GW0742, T1317/9cRA, ATRA, and dexamethasone groups; n = 2 for IFNγ). d WT and Mafb −/− macrophages were stimulated with GW0742 or T1317/9cRA. Mafb f/f and Mafb f/f::Tie2-Cre macrophages were stimulated with ATRA, dexamethasone or IFNγ. The expression of C1qa, C1qb, and C1qc was analyzed using qRT-PCR (n = 3 for the GW0742, T1317/9cRA, ATRA, and dexamethasone groups; n = 2 for IFNγ). bd The expression of target genes was normalized to Hprt mRNA. c, d The data are presented as the mean ± s.e.m. *WT vs. Mafb −/−, Mafb f/f vs. Mafb f/f::Tie2-Cre; # no treatment vs. agonist; *, # p < 0.05, **, ## p < 0.01, n.s. not significant (Student’s t-test)