Fig. 4.
Fig. 4. Fas-triggered mitochondria-dependent signaling in MDS. / (A) MNCs obtained from 10 patients with RA, 12 with RARS, and 10 with NBM were subjected to anti–Fas antibody treatment (1 μg/mL) for 4 hours, and caspase-9 activation was then evaluated. Fas ligation induced a significant increase in caspase-9 activity in RARS (P = .002) and in RA (P = .004), but not in NBM cells (P = .09). (B) Caspase-3–like activity was determined in MNCs from 10 patients with RA, 12 with RARS, and 10 with NBM incubated for 4 hours in the presence or absence of LEHD-fmk (20 μM). Fas-induced caspase-3–like activity was more prominent in RARS (P = .002) and in RA (P < .05) as compared with NBM, and this activity was suppressed by the inhibition of caspase-9 (P = .003) in both subgroups of MDS. Each line represents data obtained from one patient.

Fas-triggered mitochondria-dependent signaling in MDS.

(A) MNCs obtained from 10 patients with RA, 12 with RARS, and 10 with NBM were subjected to anti–Fas antibody treatment (1 μg/mL) for 4 hours, and caspase-9 activation was then evaluated. Fas ligation induced a significant increase in caspase-9 activity in RARS (P = .002) and in RA (P = .004), but not in NBM cells (P = .09). (B) Caspase-3–like activity was determined in MNCs from 10 patients with RA, 12 with RARS, and 10 with NBM incubated for 4 hours in the presence or absence of LEHD-fmk (20 μM). Fas-induced caspase-3–like activity was more prominent in RARS (P = .002) and in RA (P < .05) as compared with NBM, and this activity was suppressed by the inhibition of caspase-9 (P = .003) in both subgroups of MDS. Each line represents data obtained from one patient.

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