Fig. 3: The effects of conditional knockout of RGS1 in Flt3⁺ and Tie2⁺ AMs on infection, injury, and fibrosis.

The ratios of Flt3⁺/Tie2⁺ AMs (a) and PaO₂/FiO₂ (b) in RGS1^Flt3 and RGS1^Tie2 mice within 2 weeks of E. coli infection; values were compared to the corresponding Flt3-creERt2 or Tie2-creERt2 control mice. Survival curves (e) for RGS1^Flt3 and RGS1^Tie2 mice within 4 weeks of E. coli infection. Serum L-lactic acid (f) and serum D-lactic acid (g) levels in RGS1^Flt3 and RGS1^Tie2 mice at 14 days of E. coli infection. The expression of cathepsin K, MMP9, iNOS, α-SMA, collagen I, and collagen IV in the lung of RGS1^Flt3 and RGS1^Tie2 mice was compared with that in WT mice at 14 days of E. coli infection (h). The levels of released mtDNA, proteome, HMGB1, and GAPDH in BALF of RGS1^Flt3 and RGS1^Tie2 mice at 14 days of E. coli infection were determined by dot blotting, Coomassie blue staining, and western blot (i). j Lung H&E staining, lung Masson’s trichrome staining, tissue damage scores, and the blood PaO₂/FiO₂ ratio in RGS1^Flt3 and RGS1^Tie2 mice in the LPS-induced ALI model. k Lung H&E staining, lung Masson’s trichrome staining, lung collagen deposition area, and assessment of blood Rsc in RGS1^Flt3 and RGS1^Tie2 mice in the BLM-induced PF model. The data are shown as the mean ± SD; *p < 0.05 and **p < 0.01 by ANOVA. The data in a–d, j, k are based on 3 mice at each time point; the data in e are based on 8–11 mice used to assess the survival rate; the data in h, i were derived from 3 independent experiments using 3 mice.