Figure 2.
Figure 2. FVIIa prevents nuclei condensation in growth factor–deprived BHK(+TF) cells. Monolayers of BHK(+TF) cells were incubated in SFM for 6 hours (A-B) or treated with 20 nM FVIIa in SFM (C-D). At the end of the incubation, the cells were washed, fixed, permeabilized, and stained with Hoechst (A,C) or with goat anti–human TF IgG, followed by biotinylated donkey anti–goat IgG, HRP-streptavidin, and TSA-FITCH (B,D). Note the apoptotic cells (arrows) when BHK(+TF) cells were deprived of serum (A-B) compared with the inhibition of apoptosis seen by the absence of any apoptotic nuclei when treated with FVIIa (C,D). All fields are representative of multiple fields observed in 3 independent experiments. Scale bar indicates 50 μm.

FVIIa prevents nuclei condensation in growth factor–deprived BHK(+TF) cells. Monolayers of BHK(+TF) cells were incubated in SFM for 6 hours (A-B) or treated with 20 nM FVIIa in SFM (C-D). At the end of the incubation, the cells were washed, fixed, permeabilized, and stained with Hoechst (A,C) or with goat anti–human TF IgG, followed by biotinylated donkey anti–goat IgG, HRP-streptavidin, and TSA-FITCH (B,D). Note the apoptotic cells (arrows) when BHK(+TF) cells were deprived of serum (A-B) compared with the inhibition of apoptosis seen by the absence of any apoptotic nuclei when treated with FVIIa (C,D). All fields are representative of multiple fields observed in 3 independent experiments. Scale bar indicates 50 μm.

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