Fig. 2: Wound healing is coupled with increased signaling events of STING.

Male WT C57BL/6 J mice, at 4–5 weeks of age, were fed an HFD for 12 weeks, then intraperitoneally injected Streptozocin (STZ) to form a diabetes model (DM mice), 4 weeks later, all WT and DM mice were prepared 10 × 10 mm2 wounds on the backs using skin punches, then waited for natural healing. A Non-wounded and wounded back skin lysates (days 3 after trauma, indicated at the top of each lane) of WT and DM mice were examined for STING using western blot analysis. Blots are quantified using bar graphs. B Skin and wound mRNA levels were examined using RT-qPCR. C Non-wounded and wounded back skin lysates (days 3, 7, 11, 13 after trauma, indicated at the top of each lane) of WT and DM mice were examined for cGAS, STING, and IL-1β using western blot analysis. Blots are quantified using bar graphs. D Wound mRNA levels were examined using RT-qPCR. E Sections of WT (left 4 columns) and DM (right 4 columns) on days 3, 7, 11, and 13 after trauma (upper, middle 1–2, and lower row) were stained with 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). For all bar graphs, Data were represented as mean ± SD (n = 3). *P < 0.05, **P < 0.01 and ***P < 0.001, WT vs DM.