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. 2020 Sep 30;11:566410. doi: 10.3389/fphys.2020.566410

Figure 3.

Figure 3

AngII/AT1R pathway downregulates PP2Ac Tyr307 phosphorylation, which is related with ROS generation. (A,B) CAN blocked AngII-mediated downregulation of PP2Ac Tyr307 phosphorylation in HUVECs. HUVECs were pretreated with 10−6 M CAN for 3 h or not, then stimulated with 10−7 M AngII for 12 h (n = 6 independent experiments). (C,D) CAN blocked AngII-mediated downregulation of PP2Ac Tyr307 phosphorylation in rat mesenteric arteries (n = 6 rats per group). (E,F) ROS content was enhanced by AngII (10−7 M, 12 h) and abolished by pretreatment with CAN (10−6 M, 3 h). HUVECs were incubated with DCFH-DA (5 μmol/L) for 30 min, and ROS content was measure. The representative images shown were captured using a fluorescence microscope (100× magnification; n = 4 independent experiments). Pretreatment with the antioxidant, (G,H) N-acetylcysteine (NAC; 10−3 M, 1 h) and (I,J) Apocynin (APO; 2 × 10−5 M, 1 h), inhibited AngII/AT1R-mediated downregulation of PP2Ac Tyr307 and eNOS Ser1177 (n = 6 independent experiments). *p < 0.05 vs. Control or Sham group; #p < 0.05 vs. AngII group.