Skip to main content
. 2004 May 1;113(9):1318–1327. doi: 10.1172/JCI19930

Figure 2.

Figure 2

Prevention of PBEF translation with an antisense oligonucleotide blocks inhibition of apoptosis in response to inflammatory stimuli. (A) Neutrophil apoptosis, assessed as the nuclear uptake of propidium iodide, was significantly inhibited by coincubation with LPS (1 ∝g/ml), IL-1β (100 pg/ml), GM-CSF (20 ng/ml), IL-8 (250 ng/ml), or TNF-α (40 ng/ml). *P < 0.05 compared with control rates. Prevention of PBEF translation using an antisense oligonucleotide prevented this inhibitory effect; the corresponding sense or scrambled nonsense controls were without effect. Data are mean ± SD of six separate studies. (B) Antisense treatment of resting or LPS-stimulated (1 ∝g/ml) neutrophils inhibited the translation of PBEF as detected by Western blot analysis. Blot is representative of three separate studies. (C) Both LPS (1 ∝g/ml) and recombinant PBEF (50 ng/ml) inhibited phosphatidylserine exteriorization detected by the binding of FITC-labeled annexin V, an effect that was specifically blocked when neutrophils were pretreated with PBEF antisense; n = 4, *P < 0.05. rPBEF, recombinant PBEF.