Dicer1-deficient platelets are hyper reactive and prone to clot. (A-B) Flow cytometry analysis of fibrinogen binding to in vitro activated mouse platelets. Washed platelets from Dicer1^Pf4Δ/Pf4Δ or Dicer1^fl/fl mice were activated with increasing concentrations of a PAR4 agonist for 20 minutes in the presence of Alexa Fluor 488 labeled fibrinogen. (A) Mean ± SEM of the percentage of fibrinogen labeled (FIB488⁺) platelets or (B) intensity of fibrinogen 488 staining (gMFI). *P < .05; **P < .01; paired Student t test; n = 8 mice per group. (C-D) Flow cytometry analysis of JONA binding to platelets in whole blood in the presence of increasing concentrations of a PAR4 peptide. (C) Mean ± SEM of the percentage of JONA-labeled platelets or (D) the gMFI of JONA antibody staining (*P < .05; **P < .01; unpaired Student t test; n = 4 Dicer1^fl/fl and n = 3 Dicer1^Pf4Δ/Pf4Δ mice per group). (E-F) Analysis of tail-bleed time (E) and blood loss (F) after tail resection in Dicer1^Pf4Δ/Pf4Δ vs Dicer1^fl/fl mice (*P < .05; **P < .01; unpaired Student t test). (G) PE was induced in anesthetized mice of the indicated genotypes by IV injection of a solution of 60 mg/kg epinephrine and 150 mg/kg collagen. Time to death was monitored for 30 minutes. Shown is the Kaplan–Meier survival curve. *P < .05; log-rank test; n = 5 Pf4-Cre and n = 4 Dicer1^Pf4Δ/Pf4Δ mice per group.