Figure 6.

Chronic 300 nM EPI enhances expression of GRK3 and GRK2 at the membrane of SHβ₂AR4 cells via β₂-AR-dependent mechanism. Wildtype SH-SY5Y (Wt SH) and SHβ₂AR4 cells were subjected to catecholamine treatment in the presence or absence of 30 nM propranolol. Isolation of the membrane fraction and immunoblotting for GRK2 and GRK3 was conducted as described in Methods. EPI exposure significantly increased the level of GRK3 and GRK2 expressed in the membrane fractions from SHβ₂AR4 cells compared to vehicle-treated controls (*P < 0.05; n = 3). Inclusion of propranolol (P) with EPI treatment prevented the increased translocation of both GRK isoforms (^#P < 0.01 as compared to EPI treatment), while propranolol treatment alone was without effect. In contrast, EPI failed to increase mobilization of GRK to the plasma membrane of wt SH cells (n = 4–7). Data represent mean ± S.E.; comparisons were made by ANOVA with Tukey's post-hoc test.