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. 2022 Jul 4;12(11):5172–5188. doi: 10.7150/thno.71585

Figure 5.

Figure 5

S1pr2 inhibits AKT/eNOS/NO signaling pathway, and thus reduces EC migration, proliferation, and angiogenic activity. A-C. Western blotting of AKT or eNOS activation status in HUVECs and quantification in the indicated groups (n = 3). D. S1PR2 inhibits the NO production of HUVECs through AKT/eNOS signaling pathway (n = 8). E. S1PR2 inhibits the ability of proliferation of HUVECs through AKT/eNOS signaling pathway, as shown by MTT assay (n = 5). F-I, S1PR2 inhibits the ability of migration of HUVECs through AKT/eNOS signaling pathway, as shown by transwell chemotactic assay (F-G) and scratch wound healing assay (H-I) (n = 6). J-K, S1PR2 inhibits the ability of angiogenic sprouting of HUVECs through AKT/eNOS signaling pathway, as shown by fibrin gel bead sprouting assay (n = 5). L and M, S1PR2 inhibits the ability of tube formation of HUVECs through AKT/eNOS signaling pathway, as shown by tube formation assay (n = 5). LY294002 (LY), AKT inhibitor. L-NAME (LN), eNOS antagonist. O/E, overexpression. SH, shRNA. Scale Bars, 200 μm. Data are mean ± SEM. n.s indicates not significant. *P < 0.05; **P < 0.01.