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Special Issue "G Protein-Coupled Receptor and Their Kinases in Cell Biology and Disease 2.0"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 30 November 2021.

Special Issue Editor

Dr. Alessandro Cannavo
E-Mail Website
Guest Editor
Department of Translational Medical Sciences, University of Naples Federico II, 80131 Naples, Italy
Center for Translational Medicine, Temple University, Philadelphia, PA 19140, USA
Interests: Cardiovascular Disease; G protein coupled receptor; Neurodegenerative disorders; Periodontitis; Pharmacology
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Over the past three decades, since Nobel prize winners Robert Lefkowitz and Brian Kobilka characterized the structure of G protein-coupled receptors (GPCRs), plenty of clinical and pharmacological evidence has advanced our knowledge around how these receptors, and their signaling pathways, influence almost every aspect of mammals’ physiology. Indeed, GPCRs can transduce cellular signals from neurohormones, sensory stimuli, and ions, and their activity is directly modulated by GPCR kinases (GRKs) by phosphorylation and subsequent desensitization. Nevertheless, an alteration in GRKs’ expression, with subsequent GPCR dysfunction, may induce, or at least influence, the development and progression of different systemic disorders. Thus, several drugs which are able to directly inhibit or enhance GPCR signaling have been developed and are currently used in clinical practice.

This Special Issue is calling for both original articles and reviews providing to the readers of IJMS a comprehensive elucidation of GPCR and GRK functions in cell biology necessary for developing novel research approaches as well as therapeutic strategies.

Dr. Alessandro Cannavo
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 papers will be 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Cell biology
  • Cardiovascular disease
  • G protein-coupled receptor
  • GRK Ischemia
  • Neurodegeneration
  • Inflammation
  • Metabolism
  • Pharmacology

Published Papers (1 paper)

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Research

Open AccessArticle
Deregulation of Ca2+-Signaling Systems in White Adipocytes, Manifested as the Loss of Rhythmic Activity, Underlies the Development of Multiple Hormonal Resistance at Obesity and Type 2 Diabetes
Int. J. Mol. Sci. 2021, 22(10), 5109; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105109 - 12 May 2021
Viewed by 158
Abstract
Various types of cells demonstrate ubiquitous rhythmicity registered as simple and complex Ca2+-oscillations, spikes, waves, and triggering phenomena mediated by G-protein and tyrosine kinase coupled receptors. Phospholipase C/IP3-receptors (PLC/IP3R) and endothelial NO-synthase/Ryanodine receptors (NOS/RyR)–dependent Ca2+ signaling [...] Read more.
Various types of cells demonstrate ubiquitous rhythmicity registered as simple and complex Ca2+-oscillations, spikes, waves, and triggering phenomena mediated by G-protein and tyrosine kinase coupled receptors. Phospholipase C/IP3-receptors (PLC/IP3R) and endothelial NO-synthase/Ryanodine receptors (NOS/RyR)–dependent Ca2+ signaling systems, organized as multivariate positive feedback generators (PLC-G and NOS-G), underlie this rhythmicity. Loss of rhythmicity at obesity may indicate deregulation of these signaling systems. To issue the impact of cell size, receptors’ interplay, and obesity on the regulation of PLC-G and NOS-G, we applied fluorescent microscopy, immunochemical staining, and inhibitory analysis using cultured adipocytes of epididumal white adipose tissue of mice. Acetylcholine, norepinephrine, atrial natriuretic peptide, bradykinin, cholecystokinin, angiotensin II, and insulin evoked complex [Ca2+]i responses in adipocytes, implicating NOS-G or PLC-G. At low sub-threshold concentrations, acetylcholine and norepinephrine or acetylcholine and peptide hormones (in paired combinations) recruited NOS-G, based on G proteins subunits interplay and signaling amplification. Rhythmicity was cell size- dependent and disappeared in hypertrophied cells filled with lipids. Contrary to control cells, adipocytes of obese hyperglycemic and hypertensive mice, growing on glucose, did not accumulate lipids and demonstrated hormonal resistance being non responsive to any hormone applied. Preincubation of preadipocytes with palmitoyl-L-carnitine (100 nM) provided accumulation of lipids, increased expression and clustering of IP3R and RyR proteins, and partially restored hormonal sensitivity and rhythmicity (5–15% vs. 30–80% in control cells), while adipocytes of diabetic mice were not responsive at all. Here, we presented a detailed kinetic model of NOS-G and discussed its control. Collectively, we may suggest that universal mechanisms underlie loss of rhythmicity, Ca2+-signaling systems deregulation, and development of general hormonal resistance to obesity. Full article
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