Figure 5
Figure 5. Adhesion to C166 endothelial cells, expression of adhesion molecules, and DNA staining for mobilized SKL and/or KL cells. (A) Percent adhesion of mobilized SKL and KL cells to C166 endothelial cells from one of 3 experiments with similar results (left panel). The right panel shows mean fold increase in adhesion (± SEM) compared with G-CSF from 3 experiments. *P < .05. (B) Expression of CD11a, CD49d, CD49e, and CD62L on SKL cells mobilized by G-CSF and/or GROβΔ4. Mean fluorescence intensity (± SEM) of each molecule and isotype staining are shown for 3 replicates of 10 mice per group. (C) DNA histogram of KL cells mobilized by G-CSF or GROβΔ4. PBMCs were stained with antilineage antibodies (PE), c-kit (FITC), and 7-AAD. Cell cycle distribution was quantitated using ModFIT Software (Becton Dickinson).

Adhesion to C166 endothelial cells, expression of adhesion molecules, and DNA staining for mobilized SKL and/or KL cells. (A) Percent adhesion of mobilized SKL and KL cells to C166 endothelial cells from one of 3 experiments with similar results (left panel). The right panel shows mean fold increase in adhesion (± SEM) compared with G-CSF from 3 experiments. *P < .05. (B) Expression of CD11a, CD49d, CD49e, and CD62L on SKL cells mobilized by G-CSF and/or GROβΔ4. Mean fluorescence intensity (± SEM) of each molecule and isotype staining are shown for 3 replicates of 10 mice per group. (C) DNA histogram of KL cells mobilized by G-CSF or GROβΔ4. PBMCs were stained with antilineage antibodies (PE), c-kit (FITC), and 7-AAD. Cell cycle distribution was quantitated using ModFIT Software (Becton Dickinson).

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