Figure 6.
The A2 protein in endotoxemic mice modulated fibrin formation ex vivo. (A-B) Confocal images of the fibrin structure in endotoxemic plasma collected at 2 hours after the injection of the A2 variants or vehicle control were analyzed using ImageJ. (A) Notably, larger pores were observed in the resultant fibrin clot in plasma from mice treated with the WT A2 protein (right) in comparison with mice treated with vehicle control or the A2 mutant (left or middle, respectively; n = 3 unpaired subjects). Representative of 3 experiments using 3 different mice per group. Scale bars, 10 μM. (C) Plasma samples from LPS-treated mice were obtained at 2 hours after IP injection of A2 protein (4.0 mg/kg) or saline. Fibrin polymerization was measured by turbidity at 405 nm. Turbidity curves represent the average of 6 separate experiments for each condition tested: with A2 protein or saline. *P = .036 vs control or mutant, ***P < .0001. NS, not significant.

The A2 protein in endotoxemic mice modulated fibrin formation ex vivo. (A-B) Confocal images of the fibrin structure in endotoxemic plasma collected at 2 hours after the injection of the A2 variants or vehicle control were analyzed using ImageJ. (A) Notably, larger pores were observed in the resultant fibrin clot in plasma from mice treated with the WT A2 protein (right) in comparison with mice treated with vehicle control or the A2 mutant (left or middle, respectively; n = 3 unpaired subjects). Representative of 3 experiments using 3 different mice per group. Scale bars, 10 μM. (C) Plasma samples from LPS-treated mice were obtained at 2 hours after IP injection of A2 protein (4.0 mg/kg) or saline. Fibrin polymerization was measured by turbidity at 405 nm. Turbidity curves represent the average of 6 separate experiments for each condition tested: with A2 protein or saline. *P = .036 vs control or mutant, ***P < .0001. NS, not significant.

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