Figure 4
Figure 4. Normal apoptosis and function in Flip-deficient circulating neutrophils. (A) Time-dependent loss of mitochondrial transmembrane potential (Δ Ψm) was assessed by decreased Rh123 fluorescence (x-axis) and the loss of membrane integrity assessed by uptake of DAPI (y-axis). (B) The percentage of live cells is identified as Rh123+, DAPI− (n = 4 for each group); *P < .05 and **P < .01 between groups. (C) Representative myeloperoxidase staining of peripheral blood smears, observed by light microscopy (400×). Data are representative of 3 Flipf/d, LysMc/+ and sex-matched littermate controls. (D) The ability to oxidize nonfluoresent dihydrorhodamine 123 was accessed as increased mean florescence intensity after PMA activation. (E) Neutrophil degranulation was determined by increased mean florescence intensity of cell surface CD11b after PMA stimulation. The observations were obtained from 5 Flipf/d, LysMc/+ and sex-matched littermate controls.

Normal apoptosis and function in Flip-deficient circulating neutrophils. (A) Time-dependent loss of mitochondrial transmembrane potential (Δ Ψm) was assessed by decreased Rh123 fluorescence (x-axis) and the loss of membrane integrity assessed by uptake of DAPI (y-axis). (B) The percentage of live cells is identified as Rh123+, DAPI (n = 4 for each group); *P < .05 and **P < .01 between groups. (C) Representative myeloperoxidase staining of peripheral blood smears, observed by light microscopy (400×). Data are representative of 3 Flipf/d, LysMc/+ and sex-matched littermate controls. (D) The ability to oxidize nonfluoresent dihydrorhodamine 123 was accessed as increased mean florescence intensity after PMA activation. (E) Neutrophil degranulation was determined by increased mean florescence intensity of cell surface CD11b after PMA stimulation. The observations were obtained from 5 Flipf/d, LysMc/+ and sex-matched littermate controls.

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