Figure 5
Figure 5. In vivo stimulation of F36V-Mpl signaling in human lymphomyeloid (CD34+CD38−Lin−CD7−) progenitors. Each mouse (NOD/SCID/β2-microglobulin−/−) received transplants of human CD34+CD38−Lin−CD7− progenitors transduced with F36V-MPL-LUC (F36V-MPL) or F36V-LUC (F36V) control vector. Mice were treated with or without CID from day 1 until killing 35 to 49 days after transplantation. (A) In vivo longitudinal imaging of luciferase expression in 2 mice that both received transplants of human CD34+CD38−Lin−CD7− progenitors transduced with F36V-MPL. D indicates dorsal, and and V indicates ventral view of the same mouse. (B) Quantification of signal for all animals, n = 6 mice per arm, 2 independent experiments (mean, SD; P < .001 for difference between F36V-MPL with CID and all other groups). (C) Lineage analysis of human CD45+ cells in bone marrow of representative CID-treated mouse. Boxes below show percentage in each quadrant.

In vivo stimulation of F36V-Mpl signaling in human lymphomyeloid (CD34+CD38LinCD7) progenitors. Each mouse (NOD/SCID/β2-microglobulin−/−) received transplants of human CD34+CD38LinCD7 progenitors transduced with F36V-MPL-LUC (F36V-MPL) or F36V-LUC (F36V) control vector. Mice were treated with or without CID from day 1 until killing 35 to 49 days after transplantation. (A) In vivo longitudinal imaging of luciferase expression in 2 mice that both received transplants of human CD34+CD38LinCD7 progenitors transduced with F36V-MPL. D indicates dorsal, and and V indicates ventral view of the same mouse. (B) Quantification of signal for all animals, n = 6 mice per arm, 2 independent experiments (mean, SD; P < .001 for difference between F36V-MPL with CID and all other groups). (C) Lineage analysis of human CD45+ cells in bone marrow of representative CID-treated mouse. Boxes below show percentage in each quadrant.

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