Figure 1.
PF4-Actn1−/− mice recapitulate the main features of thrombocytopenia without changes in platelet turnover. (A) Mouse MKs were isolated from the BM of Actn1f/f and PF4-Actn1−/− mice by flow sorting, and the protein expression of α-actinin-1, α-actinin-4, and total α-actinin was analyzed via western blotting. β-Actin was used as a loading control. (B) Washed platelets from Actn1f/f and PF4-Actn1−/− mice were lysed, and the protein levels of α-actinin-1, α-actinin-4, and total α-actinin were analyzed via western blotting. β-Actin was used as a loading control. (C) Platelet counts in the peripheral blood of Actn1f/f (n = 28 mice) and PF4-Actn1−/− (n = 24 mice) mice. (D) Mean platelet volume in Actn1f/f (n = 28 mice) and PF4-Actn1−/− (n = 24 mice) mice. (E) TEM images of platelets from Actn1f/f and PF4-Actn1−/− mice. Representative images from 1 of 3 experiments with similar results are displayed. The scale bar is 2 μm. Male mice aged 6 to 10 weeks were used for these animal experiments. (F) The area of each platelet in cross-sections of the TEM was measured (n = 287, Actn1f/f platelets; n = 254, PF4-Actn1−/− platelets). (G) The platelet life span was measured by determining the percentage of biotin-positive platelets in vivo at the indicated time points after tail vein injection of NHS (N-hydroxysuccinimide ester)–biotin in Actn1f/f and PF4-Actn1−/− mice (n = 10 mice per group). (H) Platelet apoptosis in Actn1f/f (n = 8 mice) and PF4-Actn1−/− (n = 6 mice) mice was measured by flow cytometry. (I) The concentration of TPO in the serum of Actn1f/f (n = 14 mice) and PF4-Actn1−/− (n = 10 mice) mice. ∗P < .05; ∗∗∗P < .005. ns, not significant.

PF4-Actn1−/− mice recapitulate the main features of thrombocytopenia without changes in platelet turnover. (A) Mouse MKs were isolated from the BM of Actn1f/f and PF4-Actn1−/− mice by flow sorting, and the protein expression of α-actinin-1, α-actinin-4, and total α-actinin was analyzed via western blotting. β-Actin was used as a loading control. (B) Washed platelets from Actn1f/f and PF4-Actn1−/− mice were lysed, and the protein levels of α-actinin-1, α-actinin-4, and total α-actinin were analyzed via western blotting. β-Actin was used as a loading control. (C) Platelet counts in the peripheral blood of Actn1f/f (n = 28 mice) and PF4-Actn1−/− (n = 24 mice) mice. (D) Mean platelet volume in Actn1f/f (n = 28 mice) and PF4-Actn1−/− (n = 24 mice) mice. (E) TEM images of platelets from Actn1f/f and PF4-Actn1−/− mice. Representative images from 1 of 3 experiments with similar results are displayed. The scale bar is 2 μm. Male mice aged 6 to 10 weeks were used for these animal experiments. (F) The area of each platelet in cross-sections of the TEM was measured (n = 287, Actn1f/f platelets; n = 254, PF4-Actn1−/− platelets). (G) The platelet life span was measured by determining the percentage of biotin-positive platelets in vivo at the indicated time points after tail vein injection of NHS (N-hydroxysuccinimide ester)–biotin in Actn1f/f and PF4-Actn1−/− mice (n = 10 mice per group). (H) Platelet apoptosis in Actn1f/f (n = 8 mice) and PF4-Actn1−/− (n = 6 mice) mice was measured by flow cytometry. (I) The concentration of TPO in the serum of Actn1f/f (n = 14 mice) and PF4-Actn1−/− (n = 10 mice) mice. ∗P < .05; ∗∗∗P < .005. ns, not significant.

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