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. 2020 Jul 21;42(4):560–572. doi: 10.1038/s41401-020-0458-7

Fig. 8. Pharmacological inhibition of PTP1B reverses the effect of lowering [Cl−]i on VEGFR2 phosphorylation and angiogenesis.

Fig. 8

a HUVECs were treated with PTP1B inhibitor II (1 μmol/L) in normal Cl− or low Cl− medium for 48 h followed by VEGF (50 ng/mL) stimulation for 5 min. Western blotting analysis of VEGFR2 phosphorylation at the Tyr951, Tyr1059, Tyr1175, and Tyr1214 sites. Representative images are shown. GAPDH was used as a loading control. b–e Densitometric analysis of the phosphorylated level of VEGFR2 at the Tyr951 (b), Tyr1054/1059 (c), Tyr1175 (d), and Tyr1214 (e) sites. **P < 0.01 vs. normal Cl−; ##P < 0.01 vs. normal Cl− + VEGF; &&P < 0.01 vs. low Cl− + VEGF, n = 6. f The aortic rings were treated with VEGF (50 ng/mL) and PTP1B inhibitor II (1 μmol/L) in normal Cl− or low Cl− medium for 4 days. Microvessel growth was observed under a microscope. Scale bars = 200 µm. g Quantification of the outgrowth area. **P < 0.01 vs. normal Cl−; ##P < 0.01 vs. normal Cl− + VEGF; &&P < 0.01 vs. low Cl− + VEGF, n = 5.