Fig. 8.
Fig. 8. Decreased bax-α expression caused the delay of PMN apoptosis. / (A) Differential expression of bcl-Xl and bax-α in 4 different PMN samples (1-4) freshly isolated from the circulation ofCD18+/+ mice orCD18−/−, respectively, as measured by semiquantitative RT-PCR. (B) Alteration of the bcl-Xl/bax-α ratio on apoptosis as calculated from the mean optical density of the PCR products obtained from PMNs of 7 animals of each group. Numbers indicate the mean ratios ± SDs; **P < .005. (C) Flow cytometric analysis of the down-regulation of Bax-α in the presence of antisense oligonucleotides (bax-α-as) when compared with the effect of scrambled oligonucleotides (bax-α-sc). (D) Survival of wild-type PMNs in the presence of bax-α antisense (bax-α-as) or scrambled (bax-α-sc) oligonucleotides. Data represent means ± SDs; **P < .005; n = 10.

Decreased bax-α expression caused the delay of PMN apoptosis.

(A) Differential expression of bcl-Xl and bax-α in 4 different PMN samples (1-4) freshly isolated from the circulation ofCD18+/+ mice orCD18−/−, respectively, as measured by semiquantitative RT-PCR. (B) Alteration of the bcl-Xl/bax-α ratio on apoptosis as calculated from the mean optical density of the PCR products obtained from PMNs of 7 animals of each group. Numbers indicate the mean ratios ± SDs; **P < .005. (C) Flow cytometric analysis of the down-regulation of Bax-α in the presence of antisense oligonucleotides (bax-α-as) when compared with the effect of scrambled oligonucleotides (bax-α-sc). (D) Survival of wild-type PMNs in the presence of bax-α antisense (bax-α-as) or scrambled (bax-α-sc) oligonucleotides. Data represent means ± SDs; **P < .005; n = 10.

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