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. Author manuscript; available in PMC: 2011 Aug 20.

Published in final edited form as: Circ Res. 2010 Jun 17;107(4):501–511. doi: 10.1161/CIRCRESAHA.110.222083

(A) Schematic structure of the human 3.0 kb VCAM-1 promoter and the NBRE consensus site at −2618 bp. (B) HUVEC were infected with 50 PFU Ad-CMV-Null or Ad-CMV-NOR1 for 6 hours and recovered for 24 hours. Infected cells were transiently transfected with luciferase reporter constructs driven by the VCAM-1 wildtype promoter or the similar promoter bearing a mutation in the NBRE site. Luciferase activity was analyzed after 48 h and data are presented as mean ± SEM fold induction from three independently performed experiments (*p < 0.05 vs. empty vector; #p < 0.05 vs. pVCAM-1-WT). (C) HUVEC were stimulated with vehicle (PBS) or TNF⟨ (1 ng/ml) for ChIP assays. PCR for an unrelated promoter fragment in the ®-actin promoter served as control for specificity. The autoradiograms are representative of three independently performed experiments.

(A) Schematic structure of the human 3.0 kb VCAM-1 promoter and the NBRE consensus site at −2618 bp. (B) HUVEC were infected with 50 PFU Ad-CMV-Null or Ad-CMV-NOR1 for 6 hours and recovered for 24 hours. Infected cells were transiently transfected with luciferase reporter constructs driven by the VCAM-1 wildtype promoter or the similar promoter bearing a mutation in the NBRE site. Luciferase activity was analyzed after 48 h and data are presented as mean ± SEM fold induction from three independently performed experiments (*p < 0.05 vs. empty vector; #p < 0.05 vs. pVCAM-1-WT). (C) HUVEC were stimulated with vehicle (PBS) or TNF⟨ (1 ng/ml) for ChIP assays. PCR for an unrelated promoter fragment in the ®-actin promoter served as control for specificity. The autoradiograms are representative of three independently performed experiments.