Fig. 7.
Fig. 7. PI-3K pathway and the IGF-I–mediated rescue of Dex-induced apoptosis. / The PI-3K pathway is responsible for IGF-I–mediated rescue of Dex-induced apoptosis. Cells were starved for 1 hour and incubated in growth media with or without the PI-3K inhibitor LY294002 (10 μM), the MAPK inhibitor PD98059 (50 μM), or the p70S6 kinase inhibitor rapamycin (10 nM) for 1 hour. Culture was then continued in the presence or absence of 100 ng/mL IGF-I for 1 hour, after which Dex or control media were added to yield a final 1 μM Dex concentration. Dead cells were enumerated after 48 or 72 hours by trypan blue exclusion (panel A). Similarly treated cells were stained with annexin V and propidium iodide after incubation for 36 hours and then examined by fluorescence-activated cell sorter (FACS) (panel B). Results are presented as mean ± SE (n = 3). Data are representative of 3 separate experiments. *P < .01 versus control. **P < .001 versus control.

PI-3K pathway and the IGF-I–mediated rescue of Dex-induced apoptosis.

The PI-3K pathway is responsible for IGF-I–mediated rescue of Dex-induced apoptosis. Cells were starved for 1 hour and incubated in growth media with or without the PI-3K inhibitor LY294002 (10 μM), the MAPK inhibitor PD98059 (50 μM), or the p70S6 kinase inhibitor rapamycin (10 nM) for 1 hour. Culture was then continued in the presence or absence of 100 ng/mL IGF-I for 1 hour, after which Dex or control media were added to yield a final 1 μM Dex concentration. Dead cells were enumerated after 48 or 72 hours by trypan blue exclusion (panel A). Similarly treated cells were stained with annexin V and propidium iodide after incubation for 36 hours and then examined by fluorescence-activated cell sorter (FACS) (panel B). Results are presented as mean ± SE (n = 3). Data are representative of 3 separate experiments. *P < .01 versus control. **P < .001 versus control.

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