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Biomedicines
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Beta-Adrenergic Receptors in Physiopathology
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Beta-Adrenergic Receptors in Physiopathology

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 October 2022) | Viewed by 17252

Special Issue Editor

Dr. Federica Barbagallo

E-Mail Website
Guest Editor
Department of Experimental Medicine, Sapienza University, 00161 Rome, Italy
Interests: phosphodiesterases; beta-adrenergic receptors; cardiovascular disease

Special Issue Information

Dear Colleagues,

β-Adrenergic receptors belong to the G protein-coupled receptor (GPCR) superfamily, whose signaling plays a critical role in the regulation of the function and processes of the cardiovascular system. Their chronic stimulation occurs in heart failure, and becomes detrimental, causing dysfunction in the activation of downstream signaling and reducing cardiac performance. This evolving notion is counterintuitive to the successful use of β-blockers which favor a reduction of β-AR stimulation to preserve cardiac function, although debate regarding their molecular mechanism is ongoing.

In this Special Issue, studies with in vitro, ex vivo or in vivo models of pathologies involving β-adrenergic receptors are welcome to address novel mechanistic insights regarding β-adrenergic receptor function. Manuscripts with translational value will be particularly encouraged. We invite authors to improve the current knowledge of the expression, function, and regulation of β -adrenoceptors with original research articles or reviews summarizing the current state of the art in this field. 

Dr. Federica Barbagallo
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • β-adrenergic receptors
  • diabetes
  • aging
  • β-blockers
  • heart failure
  • signaling pathway
  • internalization
  • oxidative stress
  • mouse model
  • translational

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Published Papers (6 papers)

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Research

Jump to: Review

16 pages, 3318 KiB  
Article
β2-Adrenergic Receptor Expression and Intracellular Signaling in B Cells Are Highly Dynamic during Collagen-Induced Arthritis
by Nadine Honke, Clemens J. Wiest and Georg Pongratz
Biomedicines 2022, 10(8), 1950; https://doi.org/10.3390/biomedicines10081950 - 11 Aug 2022
Cited by 6 | Viewed by 1903
Abstract
The sympathetic nervous system (SNS) has either a pro-inflammatory or anti-inflammatory effect, depending on the stage of arthritis. In the past, treatment of arthritic B cells with a β2-adrenergic receptor (β2-ADR) agonist has been shown to attenuate arthritis. In this study, the expression [...] Read more.
The sympathetic nervous system (SNS) has either a pro-inflammatory or anti-inflammatory effect, depending on the stage of arthritis. In the past, treatment of arthritic B cells with a β2-adrenergic receptor (β2-ADR) agonist has been shown to attenuate arthritis. In this study, the expression and signaling of β2-ADR in B cells during collagen-induced arthritis (CIA) were investigated to provide an explanation of why only B cells from arthritic mice are able to improve CIA. Splenic B cells were isolated via magnetic-activated cell sorting (MACS). Adrenergic receptors on B cells and intracellular β2-ADR downstream molecules (G protein-coupled receptor kinase 2 (GRK-2), β-Arrestin 2, p38 MAPK, extracellular signal-regulated kinase 1/2 (ERK1/2) and cAMP response element-binding protein (CREB)) were analyzed at different time points in naïve and arthritic B cells with and without stimulation of β2-ADR agonist terbutaline by flow cytometry. β2-ADR-expressing B cells increase during CIA without a change in receptor density. Moreover, we observed a profound downregulation of GRK-2 shortly after induction of arthritis and an increase in β-Arrestin 2 only at late stage of arthritis. The second messengers studied (p38, ERK1/2 and CREB) followed a biphasic course, characterized by a reduction at onset and an increase in established arthritis. Stimulation of CIA B cells with the β-ADR agonist terbutaline increased pp38 MAPK independent of the timepoint, while pERK1/2 and pCREB were enhanced only in the late phase of arthritis. The phosphorylation of p38 MAPK, ERK1/2 and CREB in the late phase of arthritis was associated with increased IL-10 produced by B10 cells. The change of β2-ADR expression and signaling during sustained inflammation might be an integral part of the switch from pro- to anti-inflammatory action of sympathetic mechanisms in late arthritis. Full article
(This article belongs to the Special Issue Beta-Adrenergic Receptors in Physiopathology)
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13 pages, 2974 KiB  
Article
Impact of R-Carvedilol on β2-Adrenergic Receptor-Mediated Spontaneous Calcium Release in Human Atrial Myocytes
by Sergi Casabella-Ramón, Verónica Jiménez-Sábado, Carmen Tarifa, Sandra Casellas, Tien Tina Lu, Paloma Izquierdo-Castro, Ignasi Gich, Marcel Jiménez, Antonino Ginel, José M. Guerra, S. R. Wayne Chen, Raul Benítez and Leif Hove-Madsen
Biomedicines 2022, 10(7), 1759; https://doi.org/10.3390/biomedicines10071759 - 21 Jul 2022
Cited by 7 | Viewed by 2471
Abstract
A hallmark of atrial fibrillation is an excess of spontaneous calcium release events, which can be mimicked by β1- or β2-adrenergic stimulation. Because β1-adrenergic receptor blockers (β1-blockers) are primarily used in clinical practice, we here examined the impact of β2-adrenergic stimulation on spontaneous [...] Read more.
A hallmark of atrial fibrillation is an excess of spontaneous calcium release events, which can be mimicked by β1- or β2-adrenergic stimulation. Because β1-adrenergic receptor blockers (β1-blockers) are primarily used in clinical practice, we here examined the impact of β2-adrenergic stimulation on spontaneous calcium release and assessed whether the R- and S-enantiomers of the non-selective β- blocker carvedilol could reverse these effects. For this purpose, human atrial myocytes were isolated from patients undergoing cardiovascular surgery and subjected to confocal calcium imaging or immunofluorescent labeling of the ryanodine receptor (RyR2). Interestingly, the β2-adrenergic agonist fenoterol increased the incidence of calcium sparks and waves to levels observed with the non-specific β-adrenergic agonist isoproterenol. Moreover, fenoterol increased both the amplitude and duration of the sparks, facilitating their fusion into calcium waves. Subsequent application of the non β-blocking R-Carvedilol enantiomer reversed these effects of fenoterol in a dose-dependent manner. R-Carvedilol also reversed the fenoterol-induced phosphorylation of the RyR2 at Ser-2808 dose-dependently, and 1 µM of either R- or S-Carvedilol fully reversed the effect of fenoterol. Together, these findings demonstrate that β2-adrenergic stimulation alone stimulates RyR2 phosphorylation at Ser-2808 and spontaneous calcium release maximally, and points to carvedilol as a tool to attenuate the pathological activation of β2-receptors. Full article
(This article belongs to the Special Issue Beta-Adrenergic Receptors in Physiopathology)
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17 pages, 3497 KiB  
Article
β-Adrenergic Receptor Stimulation Maintains NCX-CaMKII Axis and Prevents Overactivation of IL6R-Signaling in Cardiomyocytes upon Increased Workload
by Ingrid Matzer, Julia Voglhuber, Mara Kiessling, Nataša Djalinac, Viktoria Trummer-Herbst, Nishani Mabotuwana, Lavinia Rech, Michael Holzer, Samuel Sossalla, Peter P. Rainer, Andreas Zirlik and Senka Ljubojevic-Holzer
Biomedicines 2022, 10(7), 1648; https://doi.org/10.3390/biomedicines10071648 - 8 Jul 2022
Cited by 2 | Viewed by 2549
Abstract
Excessive β-adrenergic stimulation and tachycardia are potent triggers of cardiac remodeling; however, their exact cellular effects remain elusive. Here, we sought to determine the potency of β-adrenergic stimulation and tachycardia to modulate gene expression profiles of cardiomyocytes. Using neonatal rat ventricular cardiomyocytes, [...] Read more.
Excessive β-adrenergic stimulation and tachycardia are potent triggers of cardiac remodeling; however, their exact cellular effects remain elusive. Here, we sought to determine the potency of β-adrenergic stimulation and tachycardia to modulate gene expression profiles of cardiomyocytes. Using neonatal rat ventricular cardiomyocytes, we showed that tachycardia caused a significant upregulation of sodium–calcium exchanger (NCX) and the activation of calcium/calmodulin-dependent kinase II (CaMKII) in the nuclear region. Acute isoprenaline treatment ameliorated NCX-upregulation and potentiated CaMKII activity, specifically on the sarcoplasmic reticulum and the nuclear envelope, while preincubation with the β-blocker propranolol abolished both isoprenaline-mediated effects. On a transcriptional level, screening for hypertrophy-related genes revealed tachycardia-induced upregulation of interleukin-6 receptor (IL6R). While isoprenaline prevented this effect, pharmacological intervention with propranolol or NCX inhibitor ORM-10962 demonstrated that simultaneous CaMKII activation on the subcellular Ca2+ stores and prevention of NCX upregulation are needed for keeping IL6R activation low. Finally, using hypertensive Dahl salt-sensitive rats, we showed that blunted β-adrenergic signaling is associated with NCX upregulation and enhanced IL6R signaling. We therefore propose a previously unrecognized protective role of β-adrenergic signaling, which is compromised in cardiac pathologies, in preventing IL6R overactivation under increased workload. A better understanding of these processes may contribute to refinement of therapeutic options for patients receiving β-blockers. Full article
(This article belongs to the Special Issue Beta-Adrenergic Receptors in Physiopathology)
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12 pages, 1685 KiB  
Article
Cell Shortening and Calcium Homeostasis Analysis in Adult Cardiomyocytes via a New Software Tool
by Lorenzo Fassina, Maria Rita Assenza, Michele Miragoli, Andrea M. Isidori, Fabio Naro and Federica Barbagallo
Biomedicines 2022, 10(3), 640; https://doi.org/10.3390/biomedicines10030640 - 10 Mar 2022
Cited by 5 | Viewed by 3206
Abstract
Intracellular calcium (Ca2+) is the central regulator of heart contractility. Indeed, it couples the electrical signal, which pervades the myocardium, with cardiomyocytes contraction. Moreover, alterations in calcium management are the main factors contributing to the mechanical and electrical dysfunction observed in [...] Read more.
Intracellular calcium (Ca2+) is the central regulator of heart contractility. Indeed, it couples the electrical signal, which pervades the myocardium, with cardiomyocytes contraction. Moreover, alterations in calcium management are the main factors contributing to the mechanical and electrical dysfunction observed in failing hearts. So, simultaneous analysis of the contractile function and intracellular Ca2+ is indispensable to evaluate cardiomyocytes activity. Intracellular Ca2+ variations and fraction shortening are commonly studied with fluorescent Ca2+ indicator dyes associated with microscopy techniques. However, tracking and dealing with multiple files manually is time-consuming and error-prone and often requires expensive apparatus and software. Here, we announce a new, user-friendly image processing and analysis tool, based on ImageJ-Fiji/MATLAB® software, to evaluate the major cardiomyocyte functional parameters. We succeeded in analyzing fractional cell shortening, Ca2+ transient amplitude, and the kinematics/dynamics parameters of mouse isolated adult cardiomyocytes. The proposed method can be applied to evaluate changes in the Ca2+ cycle and contractile behavior in genetically or pharmacologically induced disease models, in drug screening and other common applications to assess mammalian cardiomyocyte functions. Full article
(This article belongs to the Special Issue Beta-Adrenergic Receptors in Physiopathology)
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Review

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13 pages, 293 KiB  
Review
The Role of Beta-Adrenergic Receptors in Depression and Resilience
by Hongxing Zhang, Mengqiao Cui, Jun-Li Cao and Ming-Hu Han
Biomedicines 2022, 10(10), 2378; https://doi.org/10.3390/biomedicines10102378 - 23 Sep 2022
Cited by 7 | Viewed by 3163
Abstract
Norepinephrine is a catecholamine neurotransmitter that has been extensively implicated in the neurobiology of major depressive disorder (MDD). An accumulating body of evidence indicates that investigations into the action of norepinephrine at the synaptic/receptor level hold high potential for a better understanding of [...] Read more.
Norepinephrine is a catecholamine neurotransmitter that has been extensively implicated in the neurobiology of major depressive disorder (MDD). An accumulating body of evidence indicates that investigations into the action of norepinephrine at the synaptic/receptor level hold high potential for a better understanding of MDD neuropathology and introduce possibilities for developing novel treatments for depression. In this review article, we discuss recent advances in depression neuropathology and the effects of antidepressant medications based on preclinical and clinical studies related to beta-adrenergic receptor subtypes. We also highlight a beta-3 adrenergic receptor-involved mechanism that promotes stress resilience, through which antidepressant efficacy is achieved in both rodent models for depression and patients with major depression—an alternative therapeutic strategy that is conceptually different from the typical therapeutic approach in which treatment efficacy is achieved by reversing pathological alterations rather than by enhancing a good mechanism such as natural resilience. Altogether, in this review, we systematically describe the role of beta-adrenergic receptors in depression and stress resilience and provide a new avenue for developing a conceptually innovative treatment for depression. Full article
(This article belongs to the Special Issue Beta-Adrenergic Receptors in Physiopathology)
19 pages, 1804 KiB  
Review
Role of Oxidative Stress in Cardiac Dysfunction and Subcellular Defects Due to Ischemia-Reperfusion Injury
by Naranjan S. Dhalla, Anureet K. Shah, Adriana Adameova and Monika Bartekova
Biomedicines 2022, 10(7), 1473; https://doi.org/10.3390/biomedicines10071473 - 22 Jun 2022
Cited by 22 | Viewed by 2941
Abstract
Ischemia-reperfusion (I/R) injury is well-known to be associated with impaired cardiac function, massive arrhythmias, marked alterations in cardiac metabolism and irreversible ultrastructural changes in the heart. Two major mechanisms namely oxidative stress and intracellular Ca2+-overload are considered to explain I/R-induced injury [...] Read more.
Ischemia-reperfusion (I/R) injury is well-known to be associated with impaired cardiac function, massive arrhythmias, marked alterations in cardiac metabolism and irreversible ultrastructural changes in the heart. Two major mechanisms namely oxidative stress and intracellular Ca2+-overload are considered to explain I/R-induced injury to the heart. However, it is becoming apparent that oxidative stress is the most critical pathogenic factor because it produces myocardial abnormalities directly or indirectly for the occurrence of cardiac damage. Furthermore, I/R injury has been shown to generate oxidative stress by promoting the formation of different reactive oxygen species due to defects in mitochondrial function and depressions in both endogenous antioxidant levels as well as regulatory antioxidative defense systems. It has also been demonstrated to adversely affect a wide variety of metabolic pathways and targets in cardiomyocytes, various resident structures in myocardial interstitium, as well as circulating neutrophils and leukocytes. These I/R-induced alterations in addition to myocardial inflammation may cause cell death, fibrosis, inflammation, Ca2+-handling abnormalities, activation of proteases and phospholipases, as well as subcellular remodeling and depletion of energy stores in the heart. Analysis of results from isolated hearts perfused with or without some antioxidant treatments before subjecting to I/R injury has indicated that cardiac dysfunction is associated with the development of oxidative stress, intracellular Ca2+-overload and protease activation. In addition, changes in the sarcolemma and sarcoplasmic reticulum Ca2+-handling, mitochondrial oxidative phosphorylation as well as myofibrillar Ca2+-ATPase activities in I/R hearts were attenuated by pretreatment with antioxidants. The I/R-induced alterations in cardiac function were simulated upon perfusing the hearts with oxyradical generating system or oxidant. These observations support the view that oxidative stress may be intimately involved in inducing intracellular Ca2+-overload, protease activation, subcellular remodeling, and cardiac dysfunction as a consequence of I/R injury to the heart. Full article
(This article belongs to the Special Issue Beta-Adrenergic Receptors in Physiopathology)
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