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Cells
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Novel Aspects of G Protein-Coupled Receptor Signaling
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Novel Aspects of G Protein-Coupled Receptor Signaling

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (1 April 2023) | Viewed by 4112

Special Issue Editor

Dr. András Balla

E-Mail Website
Guest Editor
Department of Physiology, Semmelweis University, Faculty of Medicine, H-1094 Budapest, Hungary
Interests: physiology; signal transduction; G-protein-coupled receptors (GPCRs); angiotensin II; renin-angiotensin system (RAS)
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Members of the GPCR superfamily form the largest group of cell membrane receptors transducing a vast array of signals leading to cellular responses. Their dysfunction is responsible for numerous diseases, including cancer, and GPCRs are one of the main targets of the currently marketed drugs. GPCRs are also one of the most studied proteins in molecular pharmacology. GPCRs possess multiple conformations, signaling possibilities, and biased ligands can induce selective signaling of the receptors. Activated GPCRs are able to initiate waves of signaling events by activating G proteins, binding to β-arrestins, transactivating other receptors, and even inducing signaling with the help of some internalized receptors. The aim of this Special Issue is to provide an overview of the latest findings in the novel aspects of G protein-coupled receptor (GPCR) functions and signaling. This Special Issue of Cells, therefore, invites contributions of review articles and original research papers covering the novel, exciting aspects of GPCRs to provide a better understanding of the complexity of their functions.

Dr. András Balla
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.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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

  • G protein-coupled receptor (GPCR), signal transduction, biased agonism, functional selectivity, arrestin, receptor cross-talk, receptor dimerization

Published Papers (2 papers)

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Research

18 pages, 1726 KiB  
Article
The Expression of Cellular Prion Protein, PrPC, Favors pTau Propagation and Blocks NMDAR Signaling in Primary Cortical Neurons
by Rafael Rivas-Santisteban, Iu Raïch, David Aguinaga, Carlos A. Saura, Rafael Franco and Gemma Navarro
Cells 2023, 12(2), 283; https://doi.org/10.3390/cells12020283 - 11 Jan 2023
Cited by 2 | Viewed by 1863
Abstract
Background: The N-methyl-D-aspartate receptor (NMDAR) is a target in current treatments for Alzheimer’s disease (AD). The human prion protein (PrPC) has an important role in the pathophysiology of AD. We hypothesized that PrPC modulates NMDA signaling, thus being a process associated with Alzheimer’s [...] Read more.
Background: The N-methyl-D-aspartate receptor (NMDAR) is a target in current treatments for Alzheimer’s disease (AD). The human prion protein (PrPC) has an important role in the pathophysiology of AD. We hypothesized that PrPC modulates NMDA signaling, thus being a process associated with Alzheimer’s disease. Methods: NMDAR signaling was characterized in the absence or presence of PrPC in cAMP level determination, mitogen-activated protein kinase (MAPK) pathway and label-free assays in homologous and heterologous systems. Bioluminescence resonance energy transfer was used to detect the formation of NMDAR-PrPC complexes. AXIS™ Axon Isolation Devices were used to determine axonal transport of Tau and pTau proteins in cortical primary neurons in the absence or presence of PrPC. Finally, proximity ligation assays were used to quantify NMDA-PrPC complex formation in neuronal primary cultures isolated from APPSw/Ind transgenic mice, an Alzheimer’s disease model expressing the Indiana and Swedish mutated version of the human amyloid precursor protein (APP). Results: We discovered a direct interaction between the PrPC and the NMDAR and we found a negative modulation of NMDAR-mediated signaling due to the NMDAR-PrPC interaction. In mice primary neurons, we identified NMDA-PrPC complexes where PrPC was capable of blocking NMDAR-mediated effects. In addition, we observed how the presence of PrPC results in increased neurotoxicity and neuronal death. Similarly, in microglial primary cultures, we observed that PrPC caused a blockade of the NMDA receptor link to the MAPK signaling cascade. Interestingly, a significant increase in NMDA-PrPC macromolecular complexes was observed in cortical neurons isolated from the APPSw,Ind transgenic model of AD. Conclusions: PrPC can interact with the NMDAR, and the interaction results in the alteration of the receptor functionality. NMDAR-PrPC complexes are overexpressed in neurons of APPSw/Ind mouse brain. In addition, PrPC exacerbates axonal transport of Tau and pTau proteins. Full article
(This article belongs to the Special Issue Novel Aspects of G Protein-Coupled Receptor Signaling)
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22 pages, 3170 KiB  
Article
Dietary Zinc Differentially Regulates the Effects of the GPR39 Receptor Agonist, TC-G 1008, in the Maximal Electroshock Seizure Test and Pentylenetetrazole-Kindling Model of Epilepsy
by Urszula Doboszewska, Katarzyna Socała, Mateusz Pieróg, Dorota Nieoczym, Jan Sawicki, Adam Sajnóg, Bernadeta Szewczyk, Katarzyna Mlyniec, Ireneusz Sowa, Danuta Barałkiewicz and Piotr Wlaź
Cells 2023, 12(2), 264; https://doi.org/10.3390/cells12020264 - 9 Jan 2023
Cited by 3 | Viewed by 1915
Abstract
The G-protein coupled receptor 39 (GPR39) is gaining increasing attention as a target for future drugs, yet there are gaps in the understanding of its pharmacology. Zinc is an endogenous agonist or an allosteric modulator, while TC-G 1008 is a synthetic, small molecule [...] Read more.
The G-protein coupled receptor 39 (GPR39) is gaining increasing attention as a target for future drugs, yet there are gaps in the understanding of its pharmacology. Zinc is an endogenous agonist or an allosteric modulator, while TC-G 1008 is a synthetic, small molecule agonist. Zinc is also a positive allosteric modulator for the activity of TC-G 1008 at GPR39. Activation of GPR39 by TC-G 1008 facilitated the development of epileptogenesis in the pentylenetetrazole (PTZ)-induced kindling model of epilepsy. Congruently, TC-G 1008 decreased the seizure threshold in the maximal electroshock seizure threshold (MEST) test. Here, we investigated the effects of TC-G 1008 under the condition of zinc deficiency. Mice were fed a zinc-adequate diet (ZnA, 50 mg Zn/kg) or a zinc-deficient diet (ZnD, 3 mg Zn/kg) for 4 weeks. Following 4 weeks of dietary zinc restriction, TC-G 1008 was administered as a single dose and the MEST test was performed. Additional groups of mice began the PTZ-kindling model during which TC-G 1008 was administered repeatedly and the diet was continued. TC-G 1008 administered acutely decreased the seizure threshold in the MEST test in mice fed the ZnD diet but not in mice fed the ZnA diet. TC-G 1008 administered chronically increased the maximal seizure severity and the percentage of fully kindled mice in those fed the ZnA diet, but not in mice fed the ZnD diet. Our data showed that the amount of zinc in a diet is a factor contributing to the effects of TC-G 1008 in vivo. Full article
(This article belongs to the Special Issue Novel Aspects of G Protein-Coupled Receptor Signaling)
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