Fig. 3: Treatment with STING inhibitor/agonist promotes/worsens DW healing.

All WT and DM mice were prepared 10 × 10 mm2 wounds on the backs using skin punches, 3 days after trauma, all DW mice were intraperitoneally injected with Vehicle, DMXAA, and C-176. A Representative images of wounded skin after treatment with either vehicle or DMXAA and C-176 at days 0, 3, 7, 11, and 13 after trauma. B Percent of wound area at each time following vehicle or DMXAA and C176 treatment relative to the original wound area. Quantification of wound areas in n = 6 (Veh, DMXAA, and C176) wounds per group were performed with Fiji software. Sections of WT, DM, DM + C176, and DM + DMXAA (upper, middle 1–2, and lower row) at days 7 after trauma were stained with H&E (Columns 1 and 2 on the left) or for IL-1β expression (Columns 3 and 4 on the left) and F4/80 expression (right 2 columns) (C), and colocalization of macrophages and STING using living cell imaging microscopy. Anti-F4/80 antibody labeled Macrophages (red), anti-STING antibody labeled STING (green) and DAPI labeled nucleus (blue) (D). E Wound lysates (days 7 after trauma) of all groups (indicated at the top of each lane) were examined for cGAS, STING, IL-1β, and inflammatory signaling using western blot analysis. Blots are quantified using bar graphs. F Wound mRNA (days 7 after trauma) levels were examined using RT-qPCR. G The secretion levels of inflammatory cytokines IL-1β, TNF-α, IL-6, and IL-10 in the wound homogenates (days 7 after trauma) were detected by ELISA. For all bar graphs, Data were represented as mean ± SD (n = 6). *P < 0.05, **P < 0.01 and ***P < 0.001, DM vs DM + DMXAA, DM vs DM + C176 (in B), WT vs DM, DM vs DM + DMXAA, DM vs DM + C176 (in E–G).