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. 2017 Apr 11;8:193. doi: 10.3389/fphar.2017.00193

FIGURE 1.

FIGURE 1

Vascular endothelial growth factor (VEGF) and Ang-2 promote angiogenesis and can be modulated by inhibition. The endothelial branching observed from in vitro aortic ring angiogenesis assays in the presence of VEGF (10 ng/mL) + Ang-2 (100 ng/mL) and the addition of bevacizumab (20 μg/mL) and L1-10 (6.5 μg/mL) for 24, 48, and 72 h duration of treatment (A). An increase in endothelial branching compared to control is denoted by (∗). A reduction in endothelial branching compared to VEGF + Ang-2 is denoted by (†). Wound closure of bEND5 cells in the presence of Ang-2 (10 ng/mL) + VEGF (5 ng/mL) and the addition of bevacizumab (20 μg/mL) and L1-10 (6.5 μg/mL) in comparison to Ang-2 (10 ng/mL) and VEGF (5 ng/mL) over 24, 48, and 72 h (B). An increase in percent wound closure relative to control is denoted by (∗) and a decrease in wound closure relative to Ang-2 + VEGF is denoted by (†). Statistical evaluation was determined by student’s t-tests; ∗ and † for p < 0.05, ∗∗ and †† for p < 0.01, ∗∗∗ and ††† for p < 0.001 and ∗∗∗∗ and †††† for p < 0.0001.