Fig. 3: The ability of β2-AR to promote β1-AR endocytosis was reduced upon β1-AA stimulation. | Cell Death Discovery

Fig. 3: The ability of β2-AR to promote β1-AR endocytosis was reduced upon β1-AA stimulation.

From: Biased activation of β2-AR/Gi/GRK2 signal pathway attenuated β1-AR sustained activation induced by β1-adrenergic receptor autoantibody

Fig. 3

A The binding ability of purified β1-AR to β2-AR proteins was detected by SPR. The β2-AR protein was first coupled to the chip, and then different concentrations of β1-AR proteins were added. B SPR was used to observe the binding of β1-AA and β2-AR protein and the influence of β1-AA on the binding of β1-AR and β2-AR. C The IC50 of β1-AA on binding β1-AR and β2-AR. D, E TIRF was used to assess NE-induced β1-AR endocytosis when HL-1 cells were transfected with siRNA β2-AR or an siRNA control. Representative images and quantification of changes in β1-AR-GFP fluorescence density are shown in D and E, respectively. Scale bar = 10 μm. n = 3/group. *P vs NE, P < 0.05. F, G: Changes in β1-AR endocytosis caused by β1-AA in HL-1 cells with and without the overexpression of β2-AR-EYFP (β2-AR OE). Scale bar = 10 μm. n = 3/group. †P vs β1-AA, P < 0.05. Data in D–G were analyzed by two-way ANOVA with the Bonferroni test. H The effects of β1-AA on intracellular Ca2+ in HL-1 cells with and without the overexpression of β2-AR-EYFP (β2-AR OE). Fluo-4 (10 μM) acted as a Ca2+ indicator. n = 3/group.

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