Fig 1: TGF-β regulates the proliferation of MDMs by activating the Wnt pathway. (A-B) RNA-seq analysis of Wnt signaling pathway gene levels in BMDMs and AMs with or without TGF-β treatment (n = 4 for BMDMs, n = 3 for AMs). (C) Ctnnb1 expression in AMs and BMDMs with or without TGF-β treatment (n = 3, *p = 0.0134). (D) Percentage of Ki67+ CD64+ CD11b+ BMDMs following in vitro culture with or without Wnt3a treatment (n = 4, ***p = 0.0006). (E) Percentage of Ki67+ CD64+ CD11b+ BMDMs following in vitro culture with indicated conditions (n = 4, statistical significance was determined by one-way ANOVA followed by Sidak's multiple comparisons test. Control vs. rTGF-β ****p < 0.0001, rTGF-β vs. rTGF-β + XAV939 ****p < 0.0001). (F) Percentage of Ki67+ MDMs (gated on CD45+ Ly6G− CD64+ MerTK+ Siglec F− CD11b+ cells) in CLO-treated mice with indicated conditions (n = 5, statistical significance was determined by one-way ANOVA followed by Sidak's multiple comparisons test. CLO vs. rTGF-β *p = 0.0287, rTGF-β vs. rTGF-β + XAV939 *p = 0.0106). (G) RNA-seq analysis of Lrp5/6 expression in AMs and BMDMs (n = 3 for AMs and n = 4 for BMDMs, ****p < 0.0001, ***p = 0.0009). (H) RNA-seq analysis of Lrp5/6 expression in AMs and MDMs at day 6 post LPS (n = 3, ***p = 0.0004, ***p = 0.0015).