Figure 6.
Figure 6. Cox2 and Lox inhibitors enhance BCR-mediated growth arrest and apoptosis of WEHI-231 cells. (A) WEHI-231 cells were stimulated with 0 to 10 μg/mL anti-IgM in the absence (□) and presence of 4 μM (•) or 10 μM (▵) of NS-398 (Cox2 inhibitor) for 48 hours before levels of [3H]thymidine incorporated into DNA were determined. (B) Similarly, WEHI-231 cells were stimulated with 0 to 10 μg/mL anti-IgM in the absence (□) and presence of 1 μM(•)or10 μM(▵) EDBC (pan Lox inhibitor) for 48 hours before levels of [3H]thymidine incorporated into DNA were determined. WEHI-231-Neo (C) and -Bcl-xL (D) B cells were stimulated with 0 to 10 μg/mL anti-IgM in the absence (□) and presence of 10 μM NS-398 plus 10 μM EDBC (•) for 48 hours before levels of [3H]thymidine incorporated into DNA were determined. All data are presented as means ± SD, n = 3 from single experiments representative of at least 3 independent experiments. (E) Neo- or Bcl-xL–expressing WEHI-231 B cells were stimulated with 0 to 10 μg/mL anti-IgM in the absence and presence of 10 μM NS-398 for 24 hours before determining the percent of cells exhibiting low Δψm as described in “Materials and methods.” (F) WEHI-231-Neo (□) and -Bcl-xL (▪) B cells were stimulated with 10 μg/mL anti-IgM in the absence and presence of 10 μM NS-398 plus 10 μM EDBC for 48 hours. The percent of apoptotic cells, as indicated by PI staining of subdiploid DNA content, was then determined. WEHI-231-Neo (G) and -Bcl-xL (H) B cells were stimulated with media, 10 μg/mL anti-IgM, anti-CD40 (10 μg/mL), or anti-IgM plus anti-CD40 (anti-Ig/CD40, both at 10 μg/mL) in the absence (□) and presence of 10 μM NS-398 plus 10 μM EDBC (▪) for 48 hours before levels of [3H]thymidine incorporated into DNA were determined. Data are presented as means ± SD, n = 3 from single experiments representative of at least 3 independent experiments.

Cox2 and Lox inhibitors enhance BCR-mediated growth arrest and apoptosis of WEHI-231 cells. (A) WEHI-231 cells were stimulated with 0 to 10 μg/mL anti-IgM in the absence (□) and presence of 4 μM (•) or 10 μM (▵) of NS-398 (Cox2 inhibitor) for 48 hours before levels of [3H]thymidine incorporated into DNA were determined. (B) Similarly, WEHI-231 cells were stimulated with 0 to 10 μg/mL anti-IgM in the absence (□) and presence of 1 μM(•)or10 μM(▵) EDBC (pan Lox inhibitor) for 48 hours before levels of [3H]thymidine incorporated into DNA were determined. WEHI-231-Neo (C) and -Bcl-xL (D) B cells were stimulated with 0 to 10 μg/mL anti-IgM in the absence (□) and presence of 10 μM NS-398 plus 10 μM EDBC (•) for 48 hours before levels of [3H]thymidine incorporated into DNA were determined. All data are presented as means ± SD, n = 3 from single experiments representative of at least 3 independent experiments. (E) Neo- or Bcl-xL–expressing WEHI-231 B cells were stimulated with 0 to 10 μg/mL anti-IgM in the absence and presence of 10 μM NS-398 for 24 hours before determining the percent of cells exhibiting low Δψm as described in “Materials and methods.” (F) WEHI-231-Neo (□) and -Bcl-xL (▪) B cells were stimulated with 10 μg/mL anti-IgM in the absence and presence of 10 μM NS-398 plus 10 μM EDBC for 48 hours. The percent of apoptotic cells, as indicated by PI staining of subdiploid DNA content, was then determined. WEHI-231-Neo (G) and -Bcl-xL (H) B cells were stimulated with media, 10 μg/mL anti-IgM, anti-CD40 (10 μg/mL), or anti-IgM plus anti-CD40 (anti-Ig/CD40, both at 10 μg/mL) in the absence (□) and presence of 10 μM NS-398 plus 10 μM EDBC (▪) for 48 hours before levels of [3H]thymidine incorporated into DNA were determined. Data are presented as means ± SD, n = 3 from single experiments representative of at least 3 independent experiments.

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