Fig. 1: Monoclonal β1-AA purified from mouse-derived hybridoma cells caused long-term activation of β1-AR but restricted β1-AR endocytosis. | Cell Death Discovery

Fig. 1: Monoclonal β1-AA purified from mouse-derived hybridoma cells caused long-term activation of β1-AR but restricted β1-AR endocytosis.

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

Fig. 1

A and B NRCMs were utilized to evaluate the effects of β1-AA (+)-IgG (β1-AA-positive total IgG) isolated from HF patients and mouse-derived monoclonal β1-AA on β1-AR activation. β1-AA (-)-IgG (β1-AA-negative total IgG) from HF patients and negative IgG from healthy mice were treated as the antibody controls. NE acted as a physiological ligand control. Phe and Met were α-adrenoceptor (α-AR) and β1-AR blockers, respectively. The peptide-based on β1-AR-ECII could specifically neutralize β1-AA. Data were analyzed by two-way ANOVA, followed by a Bonferroni post hoc test. n = 4–6/group, *P vs β1-AA, †P vs β1-AA (-)-IgG (A) or negative IgG (B), ‡P vs β1-AR-ECII, P < 0.05. C HL-1 cells were incubated with Fluo-4 (10 μM) for 90 min and then treated with different stimuli to dynamically measure the intracellular Ca2+ changes. n = 3/group. D–F TIRF was used to determine the endocytosis of β1-AR on the membrane of HL-1 cells, reflected by the decreased percentage of fluorescence value of β1-AR-GFP. D is the schematic diagram of TIRF detection. E and F are typical pictures and statistical charts of the effects of different stimuli on β1-AR-GFP endocytosis, respectively. Scale bar = 10 μm. Data were analyzed by two-way ANOVA, followed by a Bonferroni test. n = 3/group. *P vs β1-AA, P < 0.05.

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