Skip to main content
. Author manuscript; available in PMC: 2016 Nov 6.
Published in final edited form as: Circ Res. 2015 Oct 5;117(11):967–977. doi: 10.1161/CIRCRESAHA.115.306919

Figure 5. FoxO4 knockdown upregulates NO and suppresses monocyte adhesion that can be rescued by ectopic expression of Arg1.

Figure 5

(A) GFP-FoxO4 was transduced into the HAECS and stimulated with or without ischemia +TNFα. (B) HAECs cells transfected with control or FoxO4 siRNA were incubated with DAF-FM DA to visualize NO production and stimulated with ischemia for 1 hr. (C) Representative micrographs of monocyte adhesion to HAECs that were transfected with control, FoxO4, or Arg1 siRNA and stimulated with or without TNFα (D) Monocyte adhesions in (C) were quantified and averaged from 4 randomly chosen fields, and expressed as percentage relative to cells transfected with control siRNA-transfected and stimulated with TNFα (n=3). *, p<0.05. (D) Control or FoxO4 siRNA-transfected HAECs were transduced with lentiviruses expressing GFP, Arg1, or FoxO4 before adhesion assays were performed in the presence or absence of TNFα. Representative micrographs from multiple experiments (N>3) and two independent siRNA duplexes were shown. (E) Monocyte adhesion from (D) was quantified and expressed as percentage relative to that of ctl-siRNA transfected and TNFα/GFP-treated cells. (n=3). *, p<0.05.