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. 2021 Mar 5;11(10):4975–4991. doi: 10.7150/thno.55074

Figure 7.

Figure 7

Wnt5a derived from CAFs activates FZD5/NF-κB/ERK signaling in endothelial cells. (A) FZD5 levels were detected by qRT-PCR in HUVECs transfected with FZD5 siRNA (siFZD5) and control cells (**p<0.01). (B) Cell invasion and tubule formation of the indicated HUVECs (control HUVECs, HUVECs treated with rWnt5a, and FZD5-silenced HUVECs under treatment with rWnt5a) were assessed (scale bar, 100 μm). (C-D) Quantification analysis of the recruitment of HUVECs (C) and the average branch number (D) of the different groups of HUVECs are shown. (E-F) HUVECs were treated with different CM. The CM was as follows: CAF CM of scramble and loss of FOSL2 or Wnt5a in CAFs, CAF CM with siFZD5, and FBS-free medium with rWnt5a. The total and phosphorylated proteins of P65/NF-κB, ERK, VEGFR2, PI3K/AKT and β-catenin in HUVECs were determined by western blotting. β-actin was used as a loading control. Levels of p-P65 and p-ERK (F) were quantified as relative pixel intensity to β-actin.