Figure 4
Induction of HIV-1 LTR activation by bryostatin.
(a) U-87 cells (2.5 × 106) were transiently transfected with pLTR-Luc (0.5 μg/106 cells) and stimulated with different doses of bryostatin and prostratin (10 μg/ml). The luciferase activity in the cell lysates was measured 24 h later. Data represent the fold induction relative to non-treated cells (mean ± S.D. of four experiments performed in triplicate; **p < 0.01). (b) U-87 cells (2.5 × 106) were transiently transfected with pLTR-Luc, treated with or without bryostatin alone or in combination with PKC and NF-κB inhibitors and assayed for luciferase activity. Data represent the fold induction relative to bryostatin treated cells (mean ± S.D. of five experiments; *p ≤ 0.05 and **p < 0.01). (c) U-87 cells were transfected with the reporter κB plasmid, stimulated with bryostatin (100 ng/ml) alone or with NF-κB inhibitors and assayed for luciferase activity. Data represent the fold induction relative to bryostatin-treated cells (mean ± S.D. of four experiments performed in triplicate; *p ≤ 0.05). (d) U-87 cells were co-transfected with the empty vector control, or IκBα, along with the pLTR-Luc reporter construct. Data represent the fold induction relative to bryostatin-treated cells transfected with the pcDNA (mean ± S.D. of three experiments performed in triplicate; *p ≤ 0.05).
