Soluble thrombomodulin and carboxypeptidase activity contribute to delayed PG. PG was measured in the presence of increasing concentrations of exogenous (A) human C-1 inhibitor and (B) human TAFI. (C-D) Plasma from CD- and HFD-fed mice were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotted with anti-thrombomodulin antibody. The major band indicated with an arrow in panel C was quantified in panel D. Each lane and dot represent a separate mouse in panels C and D, respectively. (E) TG, (F) PG, and (G) turbidity were measured in the presence of increasing concentrations of rmTM (0.31-10 nM) or PTCI (50 µg/mL). (H) PG was measured in normal mouse plasma (NPP) in the absence and presence of PTCI and anti-mouse thrombomodulin antibody (MTM-1701) or control immunoglobulin G. (I-J) PG in plasma from CD- and HFD-fed mice in the absence and presence of MTM-1701 or PTCI. In this experiment, plasmas were from mice fed CD (13% kcal fat) or HFD (60% kcal fat) for 16 weeks. (K-O) PG parameters for CD- and HFD-fed mice in the absence or presence of MTM-1701 and PTCI. All experiments were performed in 1:3 diluted plasma, triggered with 0.5 pM TF and 0.31 µg/mL rtPA (for PG and turbidity assays). Each dot represents a separate mouse. Bars indicate medians. Statistical comparisons were performed by ANOVA with Dunnett post hoc testing using CD or HFD as the index condition. P < .05, **P < .01, ***P < .001, and ****P < .0001.