Fig. 5
From: TPM1 mediates inflammation downstream of TREM2 via the PKA/CREB signaling pathway
TPM1-induced inflammation is microglia-dependent. A Retinal whole-mounts from CX3CR1CreER:Rosa26iDTR mice following tamoxifen (TAM) and subsequent diphtheria toxin (DT) treatments were stained with an antibody against Iba-1. Scale bar, 500 µm. B–D Western blot analysis (B) and quantification of TPM1 and GFAP (C, D) in microglia-depleted CX3CR1CreER:Rosa26iDTR mouse retinas following TAM and DT treatment. Data are presented as mean ± SEM and analyzed by unpaired two-tailed Student’s t test (control vs. DT treatment, **p < 0.01). n = 4 mice in each group. E Retina sections stained with an antibody against GFAP in microglia-depleted CX3CR1CreER:Rosa26iDTR mice following TAM and DT treatment. Arrowheads show activated astrocytes and Müller cells. Scale bars, 20 µm. F–K qPCR analysis of TPM1, TNF-α, IL-1β, IL-6, COX-2 and iNOS in microglia-depleted CX3CR1CreER:Rosa26iDTR mice after siCTR or siTPM1-1 treatment. Data are presented as mean ± SEM and analyzed one-way ANOVA with Tukey’s multiple comparison test (compared to Control or DT-siCTR, *p < 0.05, **p < 0.01). n = 4, 5,5 mice in Control, DT-siCTR and DT-siTPM1-1 groups, respectively