Effect of FXII knockdown on the procoagulant and prothrombotic effects of polyP in wild-type (WT) or HRG-deficient mice. Thrombin generation was measured in plasma collected 60 minutes after IP saline or polyP treatment of WT mice (A) or HRG^−/− mice (B) without (control) or with FXII knockdown by ASO treatment. N = 8 mice per group. (C) Recalcification times were measured in plasma collected 60 minutes after WT or HRG^−/− mice without or with FXII knockdown were given IP saline or polyP. N = 8 mice per group; bars represent mean ± standard deviation (SD). (D) Thrombin-antithrombin (TAT) complex levels in plasma from WT or HRG^−/− mice without (red bars) or with FXII knockdown (blue bars). N = 8 to 9 mice per group; bars represent mean ± SD. (E) Fibrin deposition (red) in lungs from WT or HRG^−/− mice without or with FXII knockdown was identified by immunofluorescence using an anti-fibrin(ogen) antibody. 4′,6-Diamidino-2-phenylindole (blue) was used as a nuclear stain. Scale bar represents 50 μm. (F) Fibrin intensities in panel E were quantified in a blinded manner by using a scale of 0 to 4. N = 8 mice per group; bars represent mean ± SD. **P < .01 compared with WT mice with FXII knockdown given saline; ^###P < .001 compared with HRG^−/− mice with FXII knockdown given saline (analysis of variance, Holm-Šídák method). NS, not significant.