Coexpression of CBP/p300 restores NF-κB transcriptional activity in APLA/anti-β₂GPI–activated endothelial cells in the presence of KLF2 or KLF4. (A) Endothelial cells were transfected with expression vectors containing scrambled DNA (Scr DNA, control) or KLF2, and/or CBP/p300. All cells were also transfected with an NF-κB–luciferase reporter and Renilla luciferase. Cells were subsequently treated with medium alone, β₂GPI (100nM)/anti-β₂GPI antibodies (600nM), or TNF-α (10 ng/mL) for 5 hours before measurement of NF-κB luciferase activity, which was normalized to Renilla. KLF2 expression inhibited NF-κB transcriptional activity in the presence of β₂GPI/anti-β₂GPI antibodies, although inhibition was reversed by CBP/p300 (*P < .005) in the presence of CBP/p300 compared with KLF2 + β₂GPI/anti-β₂GPI alone. Error bars represent the mean ± SEM of triplicate points, and data are representative of 3 independent experiments. (B) Endothelial cells were transfected with expression vectors containing scrambled DNA (Scr DNA, control) or KLF4, and/or CBP/p300. All cells were also transfected with an NF-κB–luciferase reporter and Renilla luciferase. KLF4 expression inhibited NF-κB transcriptional activity in the presence of β₂GPI and anti-β₂GPI antibodies; inhibition was partially reversed by CBP/p300 (P = .056). Error bars represent the mean ± SEM of triplicate points, and data are representative of 3 independent experiments.