Fig. 5.

PI3K/Akt/VEGF signaling pathway is involved in the pro-angiogenic effect of gastrin. Endothelial cells were incubated with gastrin at the indicated concentrations for 24 h. VEGFA (a), phospho-PI3K (b), and phospho-Akt (c) results were normalized by GAPDH, total PI3K, and Akt, respectively. Endothelial cells were treated with gastrin (100 nM, 24 h) in the presence or absence of a PI3K inhibitor, LY294003 (1000 nM). Phospho-Akt (d) and VEGFA (e) were normalized by GAPDH and total Akt, respectively. n = 4. ^*P < 0.05, vs. Control group; ^#P < 0.05, vs gastrin-treated group. f Representative images and quantification of endothelial cell migration detected by transwell migration assay. g, Representative images and quantification of endothelial cell migration detected by scratch wound-healing assay. f and g scale bar = 50 µm. n = 4. ^*P < 0.05, vs. Control group; ^#P < 0.05, vs. gastrin-treated group. VEGF, vascular endothelial growth factor; PI3K, phosphatidylinositol 3 kinase; Akt, protein kinase B; DU, density units; p, phospho