Ets-1, but not Fli-1, enhances the ability of transforming growth factor (TGF)β to induce the CCN2 promoter. A CCN2 promoter/reporter construct driven by nucleotides -805 to +17 of the CCN2 promoter was transfected into fibroblasts in the presence or absence of a 24 h treatment with 4 ng/ml TGFβ1, as indicated. Reporters were co-transfected with empty expression vector, or expression vectors encoding Ets-1 or Fli-1 (0.5 μg expression vector/well) as indicated. Average ± standard deviation (N = 6) is shown. Relative promoter expression is shown. Whereas addition of Ets-1 potentiates the TGFβ1 induction of CCN2 promoter activity (*p < 0.05), Fli-1 limits the TGFβ induction of CCN2 promoter activity relative to the induction of CCN2 promoter activity with TGFβ in the presence of co-transfected empty expression vector (**p < 0.05). Both Fli-1 and Ets-1, however, activate the CCN2 promoter in the absence of TGFβ1 (#p < 0.05). TGFβ induces the CCN2 promoter in the absence of overexpressed transcription factor (@p < 0.05) Average ± standard deviation (N = 6) of a representavtive experiment is shown. Reporter activity was adjusted for differences in transfection efficiencies among samples using a control β-galactosidase expression vector.