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. 2013 Feb 4;110(8):3161–3166. doi: 10.1073/pnas.1222051110

Fig. 3.

Fig. 3.

AMPK induction of Bcl-6 attenuates the expression of VCAM-1, MCP-1, and MCP-3. (A and B) HUVECs were transiently transfected with control or AMPKα siRNA, then treated with AICAR or metformin for 1 h. ChIP assays were performed to determine the binding of Bcl-6 to VCAM-1, MCP-1, and MCP-3 promoters (A), and the abundance of VCAM-1, MCP-1, and MCP-3 mRNA was analyzed using qPCR (B). (C) HUVECs were transfected with control or PARP-1 siRNA, and levels of VCAM-1, MCP-1, or MCP-3 mRNA were determined. (D) HUVECs were transfected with control or Bcl-6 siRNA and then treated with or without metformin. Levels of VCAM-1, MCP-1, or MCP-3 mRNA were determined. (E) HUVECs were transfected with the MCP-1-Luc reporter (50 nM). After transfection, cells were infected with Ad-AMPK-CA or Ad-AMPK-DN [5 multiplicity of infection (MOI)] and lysed; luciferase activity was then measured. (F) Effects of AMPKα, PARP-1, and Bcl-6 knockdown and AICAR or metformin treatment on monocyte attachment to HUVECs. (G) Quantification of the results in F. *P < 0.05.