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. Author manuscript; available in PMC: 2021 Aug 18.
Published in final edited form as: Hypertension. 2021 Jul 19;78(3):816–830. doi: 10.1161/HYPERTENSIONAHA.120.15423

Figure 2. Genetic inhibition of GPR35 (G-protein–coupled receptor 35) increased nitric oxide (NO) production and reduced reactive oxygen species in human aortic endothelial cells (HAECs) while improving cell functions.

Figure 2.

In HAECs, the GPR35 expression was knocked down by the transfection of an adenovirus carrying shRNA against the human GPR35 gene (Ad-sh-GPR35), or overexpressed by an adenovirus carrying human GPR35 gene (Ad-GPR35), using adenovirus carrying β-gal (Ad-β-gal) as control. Representative images are shown underneath the dot-plot figure. Scale bar=200 μm. A, Cell migration assay in HAECs with Ad-sh-GPR35 or Ad-β-gal. n=6, *P<0.05 vs Ad-β-gal. B, Three-dimensional (3D) tube formation assay in HAECs with Ad-sh-GPR35 or Ad-β-gal. Scale bar=200 μm. n=6 per group, *P<0.05 vs Ad-β-gal. Scale bar=200 μm. n=6 per group, *P<0.05 vs Ad-β-gal. C, Cell migration assay in HAECs with Ad-GPR35 or Ad-β-gal. n=5 per group, *P<0.05 vs Ad-β-gal. D, 3D tube formation assay in HAECs with Ad-GPR35 or Ad-β-gal. n=5 per group, *P<0.05 vs Ad-β-gal. E, Cell proliferation assay in HAECs with Ad-GPR35 or Ad-β-gal. n=5 per group, *P<0.05 vs Ad-β-gal. In the figures, Mann-Whitney U tests were used, horizontal lines show mean±SD.