American Society of Hematology

Figure 3

$Figure 3. AKT is activated in HSCs of FoxO3a-deficient mice during hematopoietic recovery after 5-FU–induced myelosuppressive stress. (A) (Left panel) Phospho-AKT immunostaining in BM mononuclear cells (unfractionated) or Lin−Sca-1+ cells 2 days after 5-FU injection in 8- to 12-week-old FoxO3a-deficient or wild-type mice. (Right panel) Data mean frequency (%) plus or minus SD of phospho-AKT–positive cells in Lin−Sca-1+ cells (n = 5). *P < .01. Bar represents 100 μm. (B) FoxO3a-deficient cells are hyperresponsive to G-CSF, a phenotype rescued by rapamycin treatment. Results are means plus or minus SD of the number of colonies (n = 5). *P < .01.$

AKT is activated in HSCs of FoxO3a-deficient mice during hematopoietic recovery after 5-FU–induced myelosuppressive stress. (A) (Left panel) Phospho-AKT immunostaining in BM mononuclear cells (unfractionated) or Lin⁻Sca-1⁺ cells 2 days after 5-FU injection in 8- to 12-week-old FoxO3a-deficient or wild-type mice. (Right panel) Data mean frequency (%) plus or minus SD of phospho-AKT–positive cells in Lin⁻Sca-1⁺ cells (n = 5). *P < .01. Bar represents 100 μm. (B) FoxO3a-deficient cells are hyperresponsive to G-CSF, a phenotype rescued by rapamycin treatment. Results are means plus or minus SD of the number of colonies (n = 5). *P < .01.

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