Transient Receptor Potential (TRP) Ion Channels: From Development to Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (15 February 2021) | Viewed by 7508

Special Issue Editors


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Guest Editor
Charité – Universitätsmedizin Berlin, Berlin, Germany
Interests: potassium channels; chloride channels; transient receptor potential (TRP)

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Guest Editor
Institut für Experimentelle und Klinische Pharmakologie und Toxikologie und Interfakultäres Zentrum für Pharmakogenomik und Arzneimittelforschung (ICePhA), Klinikum der Eberhard-Karls-Universität Tübingen, Tübingen, Germany
Interests: TRP channels
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Special Issue Information

Dear Colleagues,

This Special Issue aims to highlight the significant impact of proteins named transient receptor potential (TRP) ion channels, which have fundamentally reshaped our knowledge of the physiology and pathophysiology of living systems, from the subcellular and molecular domains to the intact organism, and their interaction with the environment. Originally, the first trp gene was identified in a Drosophila mutant with abnormal vision. However, only since the trp gene was cloned thirty years ago and the deduced amino acid sequence suggested that this gene encodes for a cation channel has TRP channel research witnessed a continuous ongoing boom with cloning and characterization of mammalian and human homologs of the Drosophila trp channel. Many of these channels are polymodal (i.e., they are activated by several distinct physical stimuli and more than one ligand). Subsequently, the scientific community recognized that TRP channel dysfunctions are not only causing several monogenic diseases in humans, but also contribute to many complex pathophysiological conditions by an array of multiple systemic or local mechanisms, which all contribute to polygenetic disease. Thus, TRP channels have emerged as promising novel therapeutic targets. Therefore, we explicitly place findings in this Cells Special Issue “Transient Receptor Potential (TRP) Ion Channels: From Development to Disease” that can be taken advantage of in creating new therapies for cardio-renal, vascular-metabolic, autoimmune, and neuronal diseases that continue to challenge our community. These include kidney diseases, hypertension, diabetes, ischemia-reperfusion injury, pain, inflammation, fibrosis, and edema, to name a few.

Prof. Dr. Maik Gollasch
Prof. Dr. Bernd Nürnberg
Guest Editors

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Keywords

  • TRP channels
  • TRP channels cell signaling pathways
  • isoform-specific functions
  • regulation and function of TRP channels
  • TRP channelopathies
  • disease models for studying TRP channels
  • TRP channels and diseases
  • small-molecule inhibitors
  • ageing
  • geriatrics
  • hypertension
  • kidney

Published Papers (2 papers)

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Research

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22 pages, 3929 KiB  
Article
Acid Sphingomyelinase Impacts Canonical Transient Receptor Potential Channels 6 (TRPC6) Activity in Primary Neuronal Systems
by Stefanie Zeitler, Fabian Schumacher, Juliana Monti, Daniela Anni, Debarpan Guhathakurta, Burkhard Kleuser, Kristina Friedland, Anna Fejtová, Johannes Kornhuber and Cosima Rhein
Cells 2020, 9(11), 2502; https://doi.org/10.3390/cells9112502 - 18 Nov 2020
Cited by 9 | Viewed by 2462
Abstract
The acid sphingomyelinase (ASM)/ceramide system exhibits a crucial role in the pathology of major depressive disorder (MDD). ASM hydrolyzes the abundant membrane lipid sphingomyelin to ceramide that regulates the clustering of membrane proteins via microdomain and lipid raft organization. Several commonly used antidepressants, [...] Read more.
The acid sphingomyelinase (ASM)/ceramide system exhibits a crucial role in the pathology of major depressive disorder (MDD). ASM hydrolyzes the abundant membrane lipid sphingomyelin to ceramide that regulates the clustering of membrane proteins via microdomain and lipid raft organization. Several commonly used antidepressants, such as fluoxetine, rely on the functional inhibition of ASM in terms of their antidepressive pharmacological effects. Transient receptor potential canonical 6 (TRPC6) ion channels are located in the plasma membrane of neurons and serve as receptors for hyperforin, a phytochemical constituent of the antidepressive herbal remedy St. John’s wort. TRPC6 channels are involved in the regulation of neuronal plasticity, which likely contributes to their antidepressant effect. In this work, we investigated the impact of reduced ASM activity on the TRPC6 function in neurons. A lipidomic analysis of cortical brain tissue of ASM deficient mice revealed a decrease in ceramide/sphingomyelin molar ratio and an increase in sphingosine. In neurons with ASM deletion, hyperforin-mediated Ca2+-influx via TRPC6 was decreased. Consequently, downstream activation of nuclear phospho-cAMP response element-binding protein (pCREB) was changed, a transcriptional factor involved in neuronal plasticity. Our study underlines the importance of balanced ASM activity, as well as sphingolipidome composition for optimal TRPC6 function. A better understanding of the interaction of the ASM/ceramide and TRPC6 systems could help to draw conclusions about the pathology of MDD. Full article
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Review

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16 pages, 1335 KiB  
Review
TRPing to the Point of Clarity: Understanding the Function of the Complex TRPV4 Ion Channel
by Trine L. Toft-Bertelsen and Nanna MacAulay
Cells 2021, 10(1), 165; https://doi.org/10.3390/cells10010165 - 15 Jan 2021
Cited by 35 | Viewed by 4450
Abstract
The transient receptor potential vanilloid 4 channel (TRPV4) belongs to the mammalian TRP superfamily of cation channels. TRPV4 is ubiquitously expressed, activated by a disparate array of stimuli, interacts with a multitude of proteins, and is modulated by a range of post-translational modifications, [...] Read more.
The transient receptor potential vanilloid 4 channel (TRPV4) belongs to the mammalian TRP superfamily of cation channels. TRPV4 is ubiquitously expressed, activated by a disparate array of stimuli, interacts with a multitude of proteins, and is modulated by a range of post-translational modifications, the majority of which we are only just beginning to understand. Not surprisingly, a great number of physiological roles have emerged for TRPV4, as have various disease states that are attributable to the absence, or abnormal functioning, of this ion channel. This review will highlight structural features of TRPV4, endogenous and exogenous activators of the channel, and discuss the reported roles of TRPV4 in health and disease. Full article
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