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. 2013 Jan 6;10(78):20120548. doi: 10.1098/rsif.2012.0548

Figure 3.

Figure 3.

Angiogenic effects of EF do not require VEGF binding to VEGFR2 receptor. The effects of EF on capillary morphogenesis and VEGF release into the medium were retained in the presence of VEGFR2 blocking antibody (n = 4, p < 0.05), suggesting that EF-mediated stimulation of angiogenesis does not require VEGF ligand–receptor binding (a). Treatment of endothelial cells with a potent VEGFR2 inhibitor SU5416 effectively abolished capillary morphogenesis and VEGF release (b), but not high-frequency EF-induced MEK phosphorylation, which was significantly higher in the high-frequency group even in the presence of SU5416, when compared with low-frequency and no-EF controls (c). Interestingly, the relative magnitude of high-frequency EF-induced MEK phosphorylation normalized to no-EF (0.41 ± 0.09), no-EF + SU5416 (0.25 ± 0.04), no-EF + SU5426 + VEGF (0.44 ± 0.30), respectively, did not depend on the presence of SU5416 or exogenous VEGF and remained 1.5- to twofold higher than no-EF levels (p < 0.05, n = 3). This effect was not present in the low-frequency group.