Figure 5
Figure 5. Effect of aPL Abs on TF activity in carotid artery homogenates in A2−/− mice. A2−/− or A2+/+ mice were treated with IgG-APS, IgG-NHS (A), 4C5, anti-A2 MoAb, or MuMoAbC as control (B). TF activity was determined in homogenates of carotid arteries using a chromogenic assay, and data expressed as means ± SD in pmol/mg per mL−1 protein. Experiments were assayed in duplicate and repeated thrice. ¶Statistically different from A2+/+ mice treated with IgG-NHS (A; P = .015) or MuMoAbC (B; P = .001). *Statistically different from A2+/+ mice treated with IgG-APS (A; P = .026) or 4C5 (B; P = .007). **Statistically different from A2−/− mice treated with IgG-APS (A; P = .046) or 4C5 (B; P = .002).

Effect of aPL Abs on TF activity in carotid artery homogenates in A2−/− mice. A2−/− or A2+/+ mice were treated with IgG-APS, IgG-NHS (A), 4C5, anti-A2 MoAb, or MuMoAbC as control (B). TF activity was determined in homogenates of carotid arteries using a chromogenic assay, and data expressed as means ± SD in pmol/mg per mL−1 protein. Experiments were assayed in duplicate and repeated thrice. ¶Statistically different from A2+/+ mice treated with IgG-NHS (A; P = .015) or MuMoAbC (B; P = .001). *Statistically different from A2+/+ mice treated with IgG-APS (A; P = .026) or 4C5 (B; P = .007). **Statistically different from A2−/− mice treated with IgG-APS (A; P = .046) or 4C5 (B; P = .002).

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