Figure 4.
Figure 4. C5 specifically contributes to fibrin formation in venous thrombosis. Effect of the PDI inhibitor PACMA31 on adherent (A) and transient (B) platelets, and fibrin formation (C) under an IVC stenosis condition. Mice were treated 30 minutes before surgery and imaged over 6 hours using intravital microscopy (D) (n = 3; 3-4 visual fields per mouse; mean ± SD). Scale bar: 100 μm. Consecutive measurements were compared (treatment vs dimethyl sulfoxide [DMSO] controls) by 2-way ANOVA followed by Bonferroni posttests. P < .05. Adherent (E) and transient (F) platelets, and fibrin formation (G) were compared between C5−/− mice and WT controls under an IVC stenosis condition and imaged over 6 hours using intravital microscopy (H) (n = 6; 3-4 visual fields per mouse; mean ± SD). Scale bar: 100 μm. Consecutive measurements were evaluated by 2-way ANOVA followed by Bonferroni posttest. *P < .05; **P < .01; ***P < .001. h, hour; n.s., not significant.

C5 specifically contributes to fibrin formation in venous thrombosis. Effect of the PDI inhibitor PACMA31 on adherent (A) and transient (B) platelets, and fibrin formation (C) under an IVC stenosis condition. Mice were treated 30 minutes before surgery and imaged over 6 hours using intravital microscopy (D) (n = 3; 3-4 visual fields per mouse; mean ± SD). Scale bar: 100 μm. Consecutive measurements were compared (treatment vs dimethyl sulfoxide [DMSO] controls) by 2-way ANOVA followed by Bonferroni posttests. P < .05. Adherent (E) and transient (F) platelets, and fibrin formation (G) were compared between C5−/− mice and WT controls under an IVC stenosis condition and imaged over 6 hours using intravital microscopy (H) (n = 6; 3-4 visual fields per mouse; mean ± SD). Scale bar: 100 μm. Consecutive measurements were evaluated by 2-way ANOVA followed by Bonferroni posttest. *P < .05; **P < .01; ***P < .001. h, hour; n.s., not significant.

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