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Toxins
Special Issues
G-Protein Coupled Receptors as mediators of Toxin effects
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G-Protein Coupled Receptors as mediators of Toxin effects

A special issue of Toxins (ISSN 2072-6651).

Deadline for manuscript submissions: closed (1 June 2016) | Viewed by 25434

Special Issue Editors

Prof. Dr. Azzam A. Maghazachi

E-Mail Website
Guest Editor
Department of Clinical Sciences, College of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates
Interests: cancer; oncology; multiple sclerosis; autoimmune diseases; immunology; chemokines; hematology; drug mechanisms of action (MOA)
Special Issues, Collections and Topics in MDPI journals
Dr. Sandra Gessani

E-Mail Website
Guest Editor
Center for Gender-Specific Medicine, Istituto Superiore di Sanità, 00161 Rome, Italy
Interests: diet; inflammation; colorectal cancer; adipose tissue; obesity; immune regulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

G protein-coupled receptors (GPCRs) are integral membrane proteins which perform highly important functions. For example, they bind molecules such as chemokines, lysophospholipids and sensory signal mediators, to name just few. Interactions of these molecules with GPCRs initiate several signaling cascades, including the accumulation of cyclic adenosine monophosphate, or the hydrolysis of phosphatidylinositol bisphosphate and the generation of diacylglyceride, an activator of protein kinase C. Further, such interactions activate ion channels, such as Ca+2, Cl- or K+. Bacterial toxins, which include cholera and pertussis toxins, ADP-ribosylate, and certain residues in the carboxyl terminal of GPCRs, induce various intracellular signaling molecules.  In this Special Issue of Toxins, we will consider papers dealing with the activities of molecules that interact with GPCRs in various cell types. Special emphasis will be placed on the effects of bacterial toxins in modulating such activities.

Dr. Azzam A. Maghazachi
Dr. Sandra Gessani
Guest Editors

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 double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly 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

  • bacterial toxins
  • g protein-coupled receptors
  • chemokines
  • lysophospholipids
  • sensory molecules
  • muscarinic receptors
  • coagulation factors
  • integrins
  • other molecules

Published Papers (3 papers)

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1332 KiB  
Article
Bovine Lactoferrin-Induced CCL1 Expression Involves Distinct Receptors in Monocyte-Derived Dendritic Cells and Their Monocyte Precursors
by Daniela Latorre, Nadia Pulvirenti, Daniela Angela Covino, Barbara Varano, Cristina Purificato, Gabriella Rainaldi, Maria Cristina Gauzzi, Laura Fantuzzi, Lucia Conti, Gloria Donninelli, Manuela Del Cornò, Michela Sabbatucci, Sandra Gessani and Patrizia Puddu
Toxins 2015, 7(12), 5472-5483; https://doi.org/10.3390/toxins7124897 - 17 Dec 2015
Cited by 3 | Viewed by 6184
Abstract
Lactoferrin (LF) exhibits a wide range of immunomodulatory activities including modulation of cytokine and chemokine secretion. In this study, we demonstrate that bovine LF (bLF) up-modulates, in a concentration- and time-dependent manner, CCL1 secretion in monocytes (Mo) at the early stage of differentiation [...] Read more.
Lactoferrin (LF) exhibits a wide range of immunomodulatory activities including modulation of cytokine and chemokine secretion. In this study, we demonstrate that bovine LF (bLF) up-modulates, in a concentration- and time-dependent manner, CCL1 secretion in monocytes (Mo) at the early stage of differentiation toward dendritic cells (DCs), and in fully differentiated immature Mo-derived DCs (MoDCs). In both cell types, up-modulation of CCL1 secretion is an early event following bLF-mediated enhanced accumulation of CCL1 transcripts. Notably, bLF-mediated up-regulation of CCL1 involves the engagement of distinct surface receptors in MoDCs and their Mo precursors. We show that bLF-mediated engagement of CD36 contributes to CCL1 induction in differentiating Mo. Conversely, toll-like receptor (TLR)2 blocking markedly reduces bLF-induced CCL1 production in MoDCs. These findings add further evidence for cell-specific differential responses elicited by bLF through the engagement of distinct TLRs and surface receptors. Furthermore, the different responses observed at early and late stages of Mo differentiation towards DCs may be relevant in mediating bLF effects in specific body districts, where these cell types may be differently represented in physiopathological conditions. Full article
(This article belongs to the Special Issue G-Protein Coupled Receptors as mediators of Toxin effects)
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Review

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1753 KiB  
Review
G-Protein-Coupled Receptors: Next Generation Therapeutic Targets in Head and Neck Cancer?
by Takeharu Kanazawa, Kiyoshi Misawa, Yuki Misawa, Takayuki Uehara, Hirofumi Fukushima, Gen Kusaka, Mikiko Maruta and Thomas E. Carey
Toxins 2015, 7(8), 2959-2984; https://doi.org/10.3390/toxins7082959 - 05 Aug 2015
Cited by 25 | Viewed by 6514
Abstract
Therapeutic outcome in head and neck squamous cell carcinoma (HNSCC) is poor in most advanced cases. To improve therapeutic efficiency, novel therapeutic targets and prognostic factors must be discovered. Our studies have identified several G protein-coupled receptors (GPCRs) as promising candidates. Significant epigenetic [...] Read more.
Therapeutic outcome in head and neck squamous cell carcinoma (HNSCC) is poor in most advanced cases. To improve therapeutic efficiency, novel therapeutic targets and prognostic factors must be discovered. Our studies have identified several G protein-coupled receptors (GPCRs) as promising candidates. Significant epigenetic silencing of GPCR expression occurs in HNSCC compared with normal tissue, and is significantly correlated with clinical behavior. Together with the finding that GPCR activity can suppress tumor cell growth, this indicates that GPCR expression has potential utility as a prognostic factor. In this review, we discuss the roles that galanin receptor type 1 (GALR1) and type 2 (GALR2), tachykinin receptor type 1 (TACR1), and somatostatin receptor type 1 (SST1) play in HNSCC. GALR1 inhibits proliferation of HNSCC cells though ERK1/2-mediated effects on cell cycle control proteins such as p27, p57, and cyclin D1, whereas GALR2 inhibits cell proliferation and induces apoptosis in HNSCC cells. Hypermethylation of GALR1, GALR2, TACR1, and SST1 is associated with significantly reduced disease-free survival and a higher recurrence rate. Although their overall activities varies, each of these GPCRs has value as both a prognostic factor and a therapeutic target. These data indicate that further study of GPCRs is a promising strategy that will enrich pharmacogenomics and prognostic research in HNSCC. Full article
(This article belongs to the Special Issue G-Protein Coupled Receptors as mediators of Toxin effects)
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234 KiB  
Review
Sphingomyelinase D/Ceramide 1-Phosphate in Cell Survival and Inflammation
by Io-Guané Rivera, Marta Ordoñez, Natalia Presa, Ana Gomez-Larrauri, Jorge Simón, Miguel Trueba and Antonio Gomez-Muñoz
Toxins 2015, 7(5), 1457-1466; https://doi.org/10.3390/toxins7051457 - 29 Apr 2015
Cited by 45 | Viewed by 11381
Abstract
Sphingolipids are major constituents of biological membranes of eukaryotic cells. Many studies have shown that sphingomyelin (SM) is a major phospholipid in cell bilayers and is mainly localized to the plasma membrane of cells, where it serves both as a building block for [...] Read more.
Sphingolipids are major constituents of biological membranes of eukaryotic cells. Many studies have shown that sphingomyelin (SM) is a major phospholipid in cell bilayers and is mainly localized to the plasma membrane of cells, where it serves both as a building block for cell architecture and as a precursor of bioactive sphingolipids. In particular, upregulation of (C-type) sphingomyelinases will produce ceramide, which regulates many physiological functions including apoptosis, senescence, or cell differentiation. Interestingly, the venom of some arthropodes including spiders of the genus Loxosceles, or the toxins of some bacteria such as Corynebacterium tuberculosis, or Vibrio damsela possess high levels of D-type sphingomyelinase (SMase D). This enzyme catalyzes the hydrolysis of SM to yield ceramide 1-phosphate (C1P), which promotes cell growth and survival and is a potent pro-inflammatory agent in different cell types. In particular, C1P stimulates cytosolic phospholipase A2 leading to arachidonic acid release and the subsequent formation of eicosanoids, actions that are all associated to the promotion of inflammation. In addition, C1P potently stimulates macrophage migration, which has also been associated to inflammatory responses. Interestingly, this action required the interaction of C1P with a specific plasma membrane receptor, whereas accumulation of intracellular C1P failed to stimulate chemotaxis. The C1P receptor is coupled to Gi proteins and activates of the PI3K/Akt and MEK/ERK1-2 pathways upon ligation with C1P. The proposed review will address novel aspects on the control of inflammatory responses by C1P and will highlight the molecular mechanisms whereby C1P exerts these actions. Full article
(This article belongs to the Special Issue G-Protein Coupled Receptors as mediators of Toxin effects)
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