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. Author manuscript; available in PMC: 2021 Mar 17.
Published in final edited form as: Immunity. 2020 Mar 11;52(3):475–486.e5. doi: 10.1016/j.immuni.2020.02.002

Fig. 3. Intracellular dsDNA activates cGAS-STING pathway and induces defective endothelial cell proliferation.

Fig. 3.

(A) Time course of cGAMP concentration in mouse lung tissues post-LPS (10 mg/kg, i.p,) challenge, n = 4–11. (B) cGAMP concentration in lung tissues from Casp11fl/fl and Casp11fl/fl x Cdh5-CreERT2 mice post-LPS challenge (10 mg/kg, i.p, 6 h), n = 5–8. (C &D) circulating IFN-1β concentration in LPS treated mice (10 mg/kg, i.p, 6h). (C) Casp11fl/fl vs Casp11fl/fl x Cdh5-CreERT2 mice, n = 5–8; (D) WT vs Gsdmd−/− mice, n =5. (E & F) Expression of cGAS/STING responsive genes (CXCL10, IFIT1 and IFIT3) in lung ECs isolated from Casp11fl/fl and Casp11fl/fl x Cdh5-CreERT2 mice (E) or WT and Gsdmd−/− mice (F) post LPS challenge (10 mg/kg, 6 h, i.p), n = 5–8. (G) Immuno blot analysis of protein expression in hLMVECs transfected with mtDNA (3 μg/ml, 6h), n =3. (H) Intracellular cGAMP concentration in hLMVECs transfected with the positive control plasmid DNA or mtDNA (3 μg/ml, 6h), n = 4. (I & J) hLMVECs transfected with mtDNA (0–10 μg/ml), n = 5; (I) or cGAMP (0–12 μg/ml), n = 8, (J) for 20 h followed by serum treated (10%, 8 h). Endothelial cell proliferation (BrdU+ cells) was analyzed by proliferation kit. Data are shown as mean ± SD obtained from at least three independent experiments. * P < 0.05, * * P < 0.01, * * * P < 0.001, two-tailed t-test. Please also see Figure S2 & 3.