ACC1 deficiency in platelets impaired their activation and thrombus formation under flow conditions. (A-G) Whole blood from ACC1flx/flx, GPIbα-Cre+/−, and ACC1 pKO mice was perfused over collagen 1–coated surface (50 μg/mL) at a shear rate of 1000/s. (A) Representative images of multilayered platelet thrombi, and activated αIIbβ3, CD62P, and phosphatidylserine (PS) stainings. (B-D) Platelet deposition, thrombus formation and contraction score were assessed on BF images. (E) αIIbβ3 activation was evaluated using JON/A Ab, (F) P-selectin exposure was evaluated via staining with anti-CD62P antibody, and (G) PS exposure was determined using annexin V. The results are expressed as mean ± SEM (≥4 mice per group). #P ≤ .05 relative to ACC1flx/flx mice. $P ≤ .05 relative to GPIbα-Cre+/− mice. One-way ANOVA was used for analysis. BF, brightfield; JON/A Ab, JON/A antibody; SAC, surface area covered.
Figure 6.

ACC1 deficiency in platelets impaired their activation and thrombus formation under flow conditions. (A-G) Whole blood from ACC1flx/flx, GPIbα-Cre+/−, and ACC1 pKO mice was perfused over collagen 1–coated surface (50 μg/mL) at a shear rate of 1000/s. (A) Representative images of multilayered platelet thrombi, and activated αIIbβ3, CD62P, and phosphatidylserine (PS) stainings. (B-D) Platelet deposition, thrombus formation and contraction score were assessed on BF images. (E) αIIbβ3 activation was evaluated using JON/A Ab, (F) P-selectin exposure was evaluated via staining with anti-CD62P antibody, and (G) PS exposure was determined using annexin V. The results are expressed as mean ± SEM (≥4 mice per group). #P ≤ .05 relative to ACC1flx/flx mice. $P ≤ .05 relative to GPIbα-Cre+/− mice. One-way ANOVA was used for analysis. BF, brightfield; JON/A Ab, JON/A antibody; SAC, surface area covered.

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