Journal: Nutrition & Metabolism
Article Title: High fructose induces dysfunctional vasodilatation via PP2A-mediated eNOS Ser1177 dephosphorylation
doi: 10.1186/s12986-022-00659-3
Figure Lengend Snippet: PP2A inhibitor recovers high fructose-induced dysfunction mediated by NO reduction. MVECs were pretreated with or without 20 nM OA for 1 h and then stimulated with fructose. A NO production from MVECs (after pretreatment with fructose for 24 h) (n = 4). Western blot analysis showing the protein expression of eNOS, P-eNOS (Ser1177) ( B, C ), PP2AC, and P-PP2A (Tyr307) ( D, E ) in MVECs (after pretreatment with fructose for 8 h) (n = 3). Relative protein levels of P-eNOS (Ser1177) were normalized to that of eNOS, and those of P-PP2A (Tyr307) were normalized to that of PP2AC. All data are presented as the mean ± SEM. C, control; Fru, fructose. * P < 0.05, ** P < 0.01 when compared with the respective control groups
Article Snippet: Phosphate buffer solution powder (AR0030) and β-actin (1:1000, BM0627) antibodies were purchased from Boster Company, China; eNOS (1:1000, 32027), PP2AC (1:1000, 2038S), anti-mouse (3:5000, 4408S), anti-rabbit (1:1500,7076S) were purchased from CST, United States; P-PP2A (PP2ACα, Tyr 307; 1:1000, AF4453) and P-eNOS (Ser 1177; 1:1000, AF3247) were purchased from Affinity, China.
Techniques: Western Blot, Expressing, Control