Figure 1.
Figure 1. Proplatelet formation is the dominant mode of thrombopoiesis, but there is an alternative megakaryocyte rupture mode, which produces much larger numbers of platelet-like particles. (A–G) Time-lapse images of thrombopoiesis in living BM from 6-wk-old CAG-eGFP (green) mice under steady-state conditions (A, B, F, and G) or after treatment with TPO (C; 10 µg for 5 d; A, Video 1; B, Video 2; C, Video 3; F, Videos 4 and 5; and G, Video 6). Injected fluorescent dextran (red) shows the blood flow, and Hoechst (blue) labeled the nucleus. Slice views (top in A, C, and G), voxel views (bottom in B and F), and surface views (bottom row in A, B, C, and G) show MK surfaces and particle release at the single-platelet (triangle) level. (D and E) Numbers of particles released from MKs with proplatelet formation and MK rupture thrombopoiesis, which were calculated from visuals by automatic software. n = 50 cells from 5 animals in each group. Note that MK rupture thrombopoiesis is rapid and associated with much greater numbers of released particles. (H) Automatic software analysis of thrombopoiesis mode. Calculated changes in MK perimeters and cytoplasmic GFP signal intensities are shown. The long arm projections (>50% of the length of the mean MK diameter) were identified as proplatelets and divided into short (<100 µm) and long (>100 µm) proplatelet formation. Increases in the perimeter (deformity) and decreases in GFP intensity (during rupture) were identified as the MK rupture pattern. The data shown are from a single representative experiment from among more than five cells from different animals. (I) MK dynamics in 6-wk-old CAG-eGFP mice. Short type proplatelet was dominant in the steady state. n = 50 HPFs from 5 animals in each group. *, P < 0.05 versus control mice. (J) Time-lapse images of FasL-induced apoptosis (5 µg/mouse, i.v.). Note that the entire time course was relatively slow, and was not associated with particle release. (K) Time duration of the MK rupture and proplatelet processes. The onset is defined as the increase in perimeter (irregularity), and the end as the loss of GFP intensity (cell death). n = 15 MKs from steady-state (for MK rupture) and FasL-treated mice (for apoptosis). Bars: (red) 20 µm; (blue) 5 µm.

Proplatelet formation is the dominant mode of thrombopoiesis, but there is an alternative megakaryocyte rupture mode, which produces much larger numbers of platelet-like particles. (A–G) Time-lapse images of thrombopoiesis in living BM from 6-wk-old CAG-eGFP (green) mice under steady-state conditions (A, B, F, and G) or after treatment with TPO (C; 10 µg for 5 d; A, Video 1; B, Video 2; C, Video 3; F, Videos 4 and 5; and G, Video 6). Injected fluorescent dextran (red) shows the blood flow, and Hoechst (blue) labeled the nucleus. Slice views (top in A, C, and G), voxel views (bottom in B and F), and surface views (bottom row in A, B, C, and G) show MK surfaces and particle release at the single-platelet (triangle) level. (D and E) Numbers of particles released from MKs with proplatelet formation and MK rupture thrombopoiesis, which were calculated from visuals by automatic software. n = 50 cells from 5 animals in each group. Note that MK rupture thrombopoiesis is rapid and associated with much greater numbers of released particles. (H) Automatic software analysis of thrombopoiesis mode. Calculated changes in MK perimeters and cytoplasmic GFP signal intensities are shown. The long arm projections (>50% of the length of the mean MK diameter) were identified as proplatelets and divided into short (<100 µm) and long (>100 µm) proplatelet formation. Increases in the perimeter (deformity) and decreases in GFP intensity (during rupture) were identified as the MK rupture pattern. The data shown are from a single representative experiment from among more than five cells from different animals. (I) MK dynamics in 6-wk-old CAG-eGFP mice. Short type proplatelet was dominant in the steady state. n = 50 HPFs from 5 animals in each group. *, P < 0.05 versus control mice. (J) Time-lapse images of FasL-induced apoptosis (5 µg/mouse, i.v.). Note that the entire time course was relatively slow, and was not associated with particle release. (K) Time duration of the MK rupture and proplatelet processes. The onset is defined as the increase in perimeter (irregularity), and the end as the loss of GFP intensity (cell death). n = 15 MKs from steady-state (for MK rupture) and FasL-treated mice (for apoptosis). Bars: (red) 20 µm; (blue) 5 µm.

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