ArticleCell communication and signaling : CCS2011
Impaired desensitization of a human polymorphic α2B-adrenergic receptor variant enhances its sympatho-inhibitory activity in chromaffin cells.
Article in Cell communication and signaling : CCS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Differential Modulation of Catecholamine and Adipokine Secretion by the Short Chain Fatty Acid Receptor FFAR3 and αInternational journal of molecular sciences · 2024Article
- Nicotine Diminishes Alpha2-Adrenergic Receptor-Dependent Protection Against Oxidative Stress in H9c2 Cardiomyocytes.Drug design, development and therapy · 2024Article
- Onset Mechanisms and Prognosis of Neurally Mediated Syncope.Reports (MDPI) · 2023Review
- BAY-6096: A Potent, Selective, and Highly Water-Soluble Adrenergic αJournal of medicinal chemistry · 2023Article
- Unraveling the relationships between alpha- and beta-adrenergic modulation and the risk of heart failure.Frontiers in cardiovascular medicine · 2023Article
- GRK5 is an essential co-repressor of the cardiac mineralocorticoid receptor and is selectively induced by finerenone.World journal of cardiology · 2022Article
- GTPγS Assay for Measuring Agonist-Induced Desensitization of Two Human Polymorphic AlphaMethods in molecular biology (Clifton, N.J.) · 2022Article
- Review
- Diagnosis and prevention of the vasodepressor type of neurally mediated syncope in Japanese patients.PloS one · 2021Article
- Antagonistic Roles of GRK2 and GRK5 in Cardiac Aldosterone Signaling Reveal GRK5-Mediated Cardioprotection via Mineralocorticoid Receptor Inhibition.International journal of molecular sciences · 2020Article
- G protein-coupled receptor kinases as therapeutic targets in the heart.Nature reviews. Cardiology · 2019Review
- Neurally mediated syncope diagnosis based on adenylate cyclase activity in Japanese patients.PloS one · 2019Article
- Dissociable contributions of the amygdala to the immediate and delayed effects of emotional arousal on memory.Learning & memory (Cold Spring Harbor, N.Y.) · 2018Article
- GRK2 Up-Regulation Creates a Positive Feedback Loop for Catecholamine Production in Chromaffin Cells.Molecular endocrinology (Baltimore, Md.) · 2016Article
- Article
- Adrenal adrenoceptors in heart failure.Frontiers in physiology · 2014Review
- Association of deletion allele of insertion/deletion polymorphism in α2B adrenoceptor gene and hypertension with or without type 2 diabetes mellitus.The application of clinical genetics · 2012Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundα2-adrenergic receptors (ARs) mediate many cellular actions of epinephrine and norepinephrine and inhibit their secretion from adrenal chromaffin cells. Like many other G-protein coupled receptors (GPCRs), they undergo agonist-dependent phopshorylation and desensitization by GPCR Kinases (GRKs), a phenomenon recently shown to play a major role in the sympathetic overdrive that accompanies and aggravates chronic heart failure. A deletion polymorphism in the human α2B-AR gene (Glu301-303) causes impaired agonist-promoted receptor phosphorylation and desensitization in heterologous cell lines. Given the importance of α2-ARs in regulation of catecholamine secretion from chromaffin cells, we sought to investigate, in the present study, the desensitization properties and the sympatho-inhibitory activity of this variant in a chromaffin cell line. For this purpose, we expressed this variant and its wild type counterpart in the well-established chromaffin cell line PC12, and performed receptor phosphorylation and desensitization studies, as well as in vitro catecholamine secretion assays.
resultsBoth the agonist-induced phosphorylation and agonist-dependent desensitization of the human Glu301-303 deletion polymorphic α2B-AR are significantly impaired in PC12 cells, resulting in enhanced signaling to inhibition of cholinergic-induced catecholamine secretion in vitro.
conclusionThis α2B-AR gene polymorphism (Glu301-303 deletion) might confer better protection against conditions characterized and aggravated by sympathetic/catecholaminergic overstimulation in vivo.
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