A2 reduced TBI-induced hypercoagulable and hyperfibrinolytic states. (A,B) Fibrinogen (A) and D-dimer (B) were measured in plasma from sham and TBI mice receiving either A2 or buffer control. (C) Thrombin generation was induced in plasma collected 3 hours after TBI (top: representative traces; bottom: summary of 9 experiments). (D) The time to coagulate anionic phospholipid-depleted plasma by EVs from sham mice and TBI mice receiving A2 or TBST (A-D, n = 9-15; 1-way ANOVA). (E) The PTAH stain of kidney tissue sections shows extensive fibrin deposition in the glomerular microvasculature (TBI-TBST-1, red arrows; scale bars, 100 μm) and in perivascular interstitial tissue (TBI-TBST-2, red arrows) from mice subjected to TBI, but not from sham mice (sham). The PTAH stain is less extensive in TBI mice receiving A2 (TBI-A2, red arrows). Images are representative of 12 mice/group. (F) EVs from TBI were tested for inducing clot formation before and after VWF⁺EVs were depleted; the number of remaining VWF⁻ EVs was adjusted to the predepletion level, or a VWF-blocking antibody was added (n = 12, 1-way ANOVA on ranks). (G) The tail bleeding time of sham and TBI mice receiving A2 or TBST, measured 3 hours after injury (n = 21, 1-way ANOVA).