Fig. 9.
Fig. 9. Effects of inhibitors of early stage of apoptosis on thrombin generation and fVIII binding. / Human macrophages, SMCs, or HAECs in the amount of 2 × 105/well were incubated with 100 μg/mL oxLDL in the absence or presence of BHT (open bars), desipramine (gray bars), or a general caspase inhibitor Z-VAD-FMK (hatched bars) for 12 hours at 37°C as described in “Materials and methods.” (A) Thrombin generation in the presence of inhibitors. Following incubation, the conversion of prothrombin into thrombin in the intrinsic pathway was measured as described in Figure 7. The maximal rate of thrombin formation on oxLDL-treated cells in the absence of inhibitors was arbitrary defined as 100% (control). The maximal rate of thrombin formation on oxLDL-treated cells in the presence of inhibitors is expressed as percent of control. (B) fVIII binding in the presence of inhibitors. Binding of 125I-fVIII to oxLDL-treated cells in the absence (solid bars) or presence (open bars), of BHT desipramine (gray bars), or a general caspase inhibitor Z-VAD-FMK (hatched bars) was performed as described in Figure 2. Each bar in panels A and B represents the mean ± SD of 3 determinations.

Effects of inhibitors of early stage of apoptosis on thrombin generation and fVIII binding.

Human macrophages, SMCs, or HAECs in the amount of 2 × 105/well were incubated with 100 μg/mL oxLDL in the absence or presence of BHT (open bars), desipramine (gray bars), or a general caspase inhibitor Z-VAD-FMK (hatched bars) for 12 hours at 37°C as described in “Materials and methods.” (A) Thrombin generation in the presence of inhibitors. Following incubation, the conversion of prothrombin into thrombin in the intrinsic pathway was measured as described in Figure 7. The maximal rate of thrombin formation on oxLDL-treated cells in the absence of inhibitors was arbitrary defined as 100% (control). The maximal rate of thrombin formation on oxLDL-treated cells in the presence of inhibitors is expressed as percent of control. (B) fVIII binding in the presence of inhibitors. Binding of 125I-fVIII to oxLDL-treated cells in the absence (solid bars) or presence (open bars), of BHT desipramine (gray bars), or a general caspase inhibitor Z-VAD-FMK (hatched bars) was performed as described in Figure 2. Each bar in panels A and B represents the mean ± SD of 3 determinations.

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