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. 2014 Feb 28;3(1):e000622. doi: 10.1161/JAHA.113.000622

Figure 6.

Figure 6.

Klf4 attenuated TNF‐α‐induced expression of Vcam1 in ECs. A and B, HUVECs (A) and human aortic ECs (B) were transfected with Klf4 expression plasmid or siRNA for Klf4 (siKlf4), and then treated with TNF‐α. Expression of Vcam1 was determined by real‐time RT‐PCR (n=4). *P<0.05 compared with cells without TNF‐α treatment. C, HUVECs were transfected with the Vcam1 (−1716/+119) promoter‐luciferase construct, the Vcam1 (−288/+119) promoter‐luciferase construct, or pGL3‐basic plasmid with Klf4 expression plasmid. One day after transfection, HUVECs were treated with TNF‐α for an additional 24 hours. Luciferase activity was measured and normalized to protein content (n=4). Ct indicates control; ECs, endothelial cells; HUVECs, human umbilical vein ECs; NF‐κB, nuclear factor‐κB; RT‐PCR, reverse‐transcription polymerase chain reaction; TNF‐α, tumor necrosis factor–α; Vcam1, vascular cell adhesion molecule‐1.