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. 2021 Jul 19;78(3):816–830. doi: 10.1161/HYPERTENSIONAHA.120.15423

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© 2021 The Authors.

Hypertension is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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Figure 1. — Genetic ablation of GPR35 (G-protein–coupled receptor 35) in aortic endothelial cells (ECs) improves cell functions.A, Representative fluorescent images showing characteristics of mouse aortic ECs (MAECs) by fluorescent staining of Dil-ac-LDL uptake and Ulex-lectin binding, CD31, VE-Cadherin, and eNOS (endothelial nitric oxide synthase). Scale bar, 100 μm. B, Real-time quantitative polymerase chain reaction (qPCR) confirmed the expression levels of Gpr35 in the GPR35^WT and little to no expression in the GPR35^KO MAECs. n=6–12, *P<0.05. C, Cell migration assay in GPR35^WT and GPR35^KO MAECs. n=6 per group. Scale bar, 400 μm. D, Three-dimensional (3D) tube formation assay in GPR35^WT and GPR35^KO MAECs. n=7 group. Scale bar, 400 μm. E, Cell proliferation assay in GPR35^WT and GPR35^KO MAECs. n=4 group. In B–E, Mann-Whitney U tests were used, *P<0.05 vs GPR35^WT ECs, horizontal lines show mean±SD. DAPI indicates 4’,6-diamidino-2-phenylindole.