Fig. 2

SETD7 deficiency alleviates STZ-induced endothelial impairment. WT and Setd7^−/− mice were administrated with 50 mg/kg/d STZ or sodium citrate by intraperitoneal injection for five consecutive days. A The protein expression of SETD7 in aortic tissues of WT and Setd7^−/− mice (n = 4). B Representative images of immunofluorescence SETD7-stained thoracic aorta sections isolated from WT and Setd7^−/− mice. Scale bars, 50 μm. C Representative traces of acetylcholine (Ach)-induced endothelium-dependent relaxations (EDRs) in aortae from WT and Setd7^−/− mice. D Concentration-response curves of Ach-induced EDRs in aortae from WT and Setd7^−/− mice (n = 6). E The protein expression of eNOS, VE-cadherin, and VEGF-α in aortic tissues of WT and Setd7^−/− mice (n = 4). F Representative images of the new vessel sprouting from the isolated thoracic aortic rings of WT and Setd7^−/− mice in the presence and absence of high glucose (HG, 22 mM) for 7–10 days (n = 3). The new vessel sprouting was photographed and quantitated at 7, and 10 days of culture (40 ×). Statistical significances were calculated using (A) one-way ANOVA, (D-F) two-way ANOVA, Tukey’s multiple comparisons tests. Data are expressed as the mean ± SEM, statistical analysis revealed a significant difference with **p < 0.01 and ***p < 0.001, #p < 0.05, ##p < 0.01, ##p < 0.01, and ###p < 0.001