Figure 5.
Platelet aggregates formation onto type I collagen matrices under flow is impaired in the absence of α4A- and β1-tubulins. (A) Representative DIC micrographs of aggregates formed after perfusion of hirudinated blood of WT, KOA4A (A4A), KOB1 (B1), DKO, and romiplostim-treated DKO (DKO+R) mice for 105 seconds at 3000 reciprocal seconds (s-1) into type-I collagen-coated (200 μg/mL) polydimethylsiloxane channels. Scale bar, 50 μm. (B) Bar graph representing the mean surface ±SEM of WT, KOA4A (A4A), KOB1 (B1), and DKO mice and romiplostim-treated DKO aggregates formed under the same condition. Results are expressed in μm2. Each symbol indicates an individual flow. N ≥ 3 per group, with at least 250 aggregates counted per individual flow. Statistical analysis was conducted by 1-way ANOVA followed by Tukey HSD post-hoc test.

Platelet aggregates formation onto type I collagen matrices under flow is impaired in the absence of α4A- and β1-tubulins. (A) Representative DIC micrographs of aggregates formed after perfusion of hirudinated blood of WT, KOA4A (A4A), KOB1 (B1), DKO, and romiplostim-treated DKO (DKO+R) mice for 105 seconds at 3000 reciprocal seconds (s-1) into type-I collagen-coated (200 μg/mL) polydimethylsiloxane channels. Scale bar, 50 μm. (B) Bar graph representing the mean surface ±SEM of WT, KOA4A (A4A), KOB1 (B1), and DKO mice and romiplostim-treated DKO aggregates formed under the same condition. Results are expressed in μm2. Each symbol indicates an individual flow. N ≥ 3 per group, with at least 250 aggregates counted per individual flow. Statistical analysis was conducted by 1-way ANOVA followed by Tukey HSD post-hoc test.

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