Eight-week-old heterozygous (mTF^+/−, hTF⁺) and low TF (mTF^−/−, hTF+) female mice were lethally irradiated and transplanted with BM from WT (n = 6-8) and BERK (n = 12) mice. Blood and tissues were collected 4 months after transplantation and assessed for plasma levels of (A) TAT, (B) sVCAM-1, and (C) MPO levels in lung and (D) plasma levels of IL-6. (E) The HW:BW and (F) representative images of hearts from control Het or low TF mice transplanted with BM from either WT (WT^BM) or BERK mice (BERK^BM). (G) In a separate study, 8-week-old mice (both males and females) with EC-specific deletion of TF (TF^flox/flox, Tie 2 Cre⁺) or controls (TF^flox/flox, Tie 2 Cre⁻) were irradiated and transplanted with WT^BM (n = 10-12) or BERK^BM (n = 12-13) and HW:BW was determined 4 months later. HW:BW was also assessed in 4-month-old BERK AA (n = 9-10) and BERK SS (n = 10-12) mice (both males and females) that were fed for 10 days with chow containing (H) rivaroxaban (0.2 mg/g chow) or (I) dabigatran (10 mg/g chow), as previously described.²  Data are presented as mean ± standard error of the mean. Asterisks above bars indicate significance vs WT^BM or BERK AA within the same genotype or treatment group, respectively. Data were analyzed by 2-way analysis of variance followed by Bonferroni post-hoc analysis: *P < .05, **P < .01, ***P < .001. (J) Proposed model of cell type–specific contribution of TF to vascular inflammation and heart hypertrophy via both thrombin-dependent and thrombin-independent mechanisms. Dab, dabigatran; Δ, deletion; Riv, rivaroxaban.