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Differential Downregulation of β 1 ‐Adrenergic Receptor Signaling in the Heart

Xu, Bing, Bahriz, Sherif, Salemme, Victoria R., Wang, Ying, Zhu, Chaoqun, Zhao, Meimi, Xiang, Yang K.·2024·Journal of the American Heart Association
DOI 10.1161/jaha.123.033733
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Abstract

Background: Chronic sympathetic stimulation drives desensitization and downregulation of β1 adrenergic receptor (β 1 AR) in heart failure. We aim to explore the differential downregulation subcellular pools of β 1 AR signaling in the heart. Methods and Results: We applied chronic infusion of isoproterenol to induced cardiomyopathy in male C57BL/6J mice. We applied confocal and proximity ligation assay to examine β 1 AR association with L‐type calcium channel, ryanodine receptor 2, and SERCA2a ((Sarco)endoplasmic reticulum calcium ATPase 2a) and Förster resonance energy transfer‐based biosensors to probe subcellular β 1 AR‐PKA (protein kinase A) signaling in ventricular myocytes. Chronic infusion of isoproterenol led to reduced β 1 AR protein levels, receptor association with L‐type calcium channel and ryanodine receptor 2 measured by proximity ligation (puncta/cell, 29.65 saline versus 14.17 isoproterenol, P <0.05), and receptor‐induced PKA signaling at the plasma membrane (Förster resonance energy transfer, 28.9% saline versus 1.9% isoproterenol, P <0.05) and ryanodine receptor 2 complex (Förster resonance energy transfer, 30.2% saline versus 10.6% isoproterenol, P <0.05). However, the β 1 AR association with SERCA2a was enhanced (puncta/cell, 51.4 saline versus 87.5 isoproterenol, P <0.05), and the receptor signal was minimally affected. The isoproterenol‐infused hearts displayed decreased PDE4D (phosphodiesterase 4D) and PDE3A and increased PDE2A, PDE4A, and PDE4B protein levels. We observed a reduced role of PDE4 and enhanced roles of PDE2 and PDE3 on the β 1 AR‐PKA activity at the ryanodine receptor 2 complexes and myocyte shortening. Despite the enhanced β 1 AR association with SERCA2a, the endogenous norepinephrine‐induced signaling was reduced at the SERCA2a complexes. Inhibiting monoamine oxidase A rescued the norepinephrine‐induced PKA signaling at the SERCA2a and myocyte shortening. Conclusions: This study reveals distinct mechanisms for the downregulation of subcellular β 1 AR signaling in the heart under chronic adrenergic stimulation.

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Cited by 5

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Metadata

Authors
Xu, B., Bahriz, S., Salemme, V. R., Wang, Y., Zhu, C., Zhao, M., & Xiang, Y. K.
Venue
Journal of the American Heart Association
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2024-06-18
Volume
13
Issue
12
ISSN
2047-9980
DOI
10.1161/jaha.123.033733
Cited by
5
Language
en

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CoChat. (2026). Citation check: Differential Downregulation of β 1 ‐Adrenergic Receptor Signaling in the Heart. https://app.cochat.ai/papers/10.1161/jaha.123.033733
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Xu, B., Bahriz, S., Salemme, V. R., Wang, Y., Zhu, C., Zhao, M., & Xiang, Y. K. (2024). Differential Downregulation of β 1 ‐Adrenergic Receptor Signaling in the Heart. Journal of the American Heart Association. https://doi.org/10.1161/jaha.123.033733

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