Figure 5
ROS are produced by c-Met by mTOR-mediated inhibition of FOXO3a. (A) Mice were injected with HGF or with G-CSF with vehicle or with PHA, and the BM transcriptional levels of FOXO3a, FOXO1, and FOXO4 mRNA were determined. (B) Catalase mRNA levels in the BM of mice receiving HGF or G-CSF or G-CSF and c-Met inhibitor. (C-H) Mice were injected with rapamycin or HGF alone or in combination with rapamycin. The levels of circulating leukocytes (C), progenitors (D), and primitive SKL cells (E-F) were evaluated. (G) BM FOXO3a and (H) catalase transcriptional levels in the BM of control mice or mice injected with HGF with or without rapamycin. Values represent the mean ± SE of ≥ 3 independent experiments, 6 mice in each group. (I-J) Percentage of Lin−/c-kit+/phosphor-Thr32-FOXO3a+ cells in the BM (I) and peripheral blood (J) after treatment with G-CSF alone or in combination with rapamycin. ** P < .001; * P < .05.

ROS are produced by c-Met by mTOR-mediated inhibition of FOXO3a. (A) Mice were injected with HGF or with G-CSF with vehicle or with PHA, and the BM transcriptional levels of FOXO3a, FOXO1, and FOXO4 mRNA were determined. (B) Catalase mRNA levels in the BM of mice receiving HGF or G-CSF or G-CSF and c-Met inhibitor. (C-H) Mice were injected with rapamycin or HGF alone or in combination with rapamycin. The levels of circulating leukocytes (C), progenitors (D), and primitive SKL cells (E-F) were evaluated. (G) BM FOXO3a and (H) catalase transcriptional levels in the BM of control mice or mice injected with HGF with or without rapamycin. Values represent the mean ± SE of ≥ 3 independent experiments, 6 mice in each group. (I-J) Percentage of Lin/c-kit+/phosphor-Thr32-FOXO3a+ cells in the BM (I) and peripheral blood (J) after treatment with G-CSF alone or in combination with rapamycin. ** P < .001; * P < .05.

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