Isoproterenol Induces Vascular Oxidative Stress and Endothelial Dysfunction via a Giα-Coupled β2-Adrenoceptor Signaling Pathway
Figure 4
Isoproterenol treatment induces β2-AR-Gi-ERK1/2 pathway activation and eNOS uncoupling.
Protein expression of Giα-1,2 (A), Giα-3 (B), ERK 1/2 phosphorylated at Thr202 and Tyr204 (C), p38 MAPK phosphorylated at Thr180 and Tyr182 (D) and eNOS protein dimerization (E) in aortas from control and 7-day isoproterenol-treated (ISO) wild-type (WT) and β2KO mice. The top panels in each graph represent typical Western-blot autoradiographs. Giα protein expression was normalized to the α-actin content in each sample, and phosphorylated ERK 1/2 and p38 MAPK were normalized to the total content of ERK 1/2 and p38 MAPK, respectively, and these results were expressed as the fold-change compared to WT aorta. eNOS dimerization was expressed as ratio of dimer:monomer band intensity. The number of animals used in each group is indicated in the bars. Values are presented as the mean ± SEM. Significance was assessed using a 2-way ANOVA: *p<0.05 vs. WT.