Special Issue "Transient Receptor Potential (TRP) Channels"

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

Deadline for manuscript submissions: closed (28 February 2014)

Special Issue Editor

Guest Editor
Dr. Loren W. Runnels

Department of Pharmacology, Rutgers Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854, USA
Website | E-Mail
Interests: TRPM6 and TRPM7 ion channels; cell migration; development

Special Issue Information

Dear Colleagues,

Since the original cloning of the transient receptor potential (TRP) ion channel by Montell and Rubin in Drosophila melanogaster in 1989, the TRP ion channel family has grown to encompass seven subfamilies linked together primarily by their sequence homology: TRPC (“canonical”), TRPM (“melastatin”), TRPV (“vanilloid”), TRPA (“ankyrin”), TRPML (“mucolipin”), TRPP (or PKD for “polycystin”), and TRPN (“NOMPC-like”), which is only found in invertebrates and fish. TRP ion channels are widely expressed in many tissues and cell types, and have been shown to affect a broad range of cellular processes, including cell division, cell migration, and stress responses. These ion channels are also involved in the ability of cells to sense and respond to external stimuli, such as temperature, pH, and osmolarity. When activated, most TRP channels conduct cations to depolarize cells, so as to initiate a plethora of cellular responses. However, recent research has revealed important new functions for TRP ion channels in intracellular compartments. This Special Issue will provide an opportunity to publish open access research work and review articles related to the TRP channel family, and will offer comprehensive new insights into current developments within this exciting and important research field.

Dr. Loren W. Runnels
Guest Editor

Submission

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Keywords

  • TRP
  • ion channel
  • calcium
  • magnesium
  • zinc
  • cellular regulation
  • signal transduction
  • development

Published Papers (16 papers)

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Research

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Open AccessArticle Unique Responses are Observed in Transient Receptor Potential Ankyrin 1 and Vanilloid 1 (TRPA1 and TRPV1) Co-Expressing Cells
Cells 2014, 3(2), 616-626; doi:10.3390/cells3020616
Received: 4 April 2014 / Revised: 29 May 2014 / Accepted: 30 May 2014 / Published: 11 June 2014
Cited by 5 | PDF Full-text (412 KB) | HTML Full-text | XML Full-text | Correction
Abstract
Transient receptor potential (TRP) ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) receptors are implicated in modulation of cough and nociception. In vivo, TRPA1 and TRPV1 are often co-expressed in neurons and TRPA1V1 hetero-tetramer formation is noted in cells co-transfected with the respective
[...] Read more.
Transient receptor potential (TRP) ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) receptors are implicated in modulation of cough and nociception. In vivo, TRPA1 and TRPV1 are often co-expressed in neurons and TRPA1V1 hetero-tetramer formation is noted in cells co-transfected with the respective expression plasmids. In order to understand the impact of TRP receptor interaction on activity, we created stable cell lines expressing the TRPA1, TRPV1 and co-expressing the TRPA1 and TRPV1 (TRPA1V1) receptors. Among the 600 compounds screened against these receptors, we observed a number of compounds that activated the TRPA1, TRPV1 and TRPA1V1 receptors; compounds that activated TRPA1 and TRPA1V1; compounds that activated TRPV1 and TRPA1V1; compounds in which TRPA1V1 response was modulated by either TRPA1 or TRPV1; and compounds that activated only TRPV1 or TRPA1 or TRPA1V1; and one compound that activated TRPA1 and TRPV1, but not TRPA1V1. These results suggest that co-expression of TRPA1 and TRPV1 receptors imparts unique activation profiles different from that of cells expressing only TRPA1 or TRPV1. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessArticle Aberrantly Over-Expressed TRPM8 Channels in Pancreatic Adenocarcinoma: Correlation with Tumor Size/Stage and Requirement for Cancer Cells Invasion
Cells 2014, 3(2), 500-516; doi:10.3390/cells3020500
Received: 10 March 2014 / Revised: 7 May 2014 / Accepted: 14 May 2014 / Published: 23 May 2014
Cited by 3 | PDF Full-text (1463 KB) | HTML Full-text | XML Full-text
Abstract
The transient receptor potential melastatin-subfamily member 8 (TRPM8) channels control Ca2+ homeostasis. Recent studies indicate that TRPM8 channels are aberrantly expressed and required for cellular proliferation in pancreatic adenocarcinoma. However, the functional significance of TRPM8 in pancreatic tissues is mostly unknown. The
[...] Read more.
The transient receptor potential melastatin-subfamily member 8 (TRPM8) channels control Ca2+ homeostasis. Recent studies indicate that TRPM8 channels are aberrantly expressed and required for cellular proliferation in pancreatic adenocarcinoma. However, the functional significance of TRPM8 in pancreatic tissues is mostly unknown. The objectives of this study are to examine the expression of TRPM8 in various histopathological types of pancreatic tissues, determine its clinical significance in pancreatic adenocarcinoma, and investigate its functional role in cancer cells invasion. We present evidence that, in normal pancreatic tissues, anti-TRPM8 immunoreactivity is detected in the centroacinar cells and the islet endocrine cells. In pre-malignant pancreatic tissues and malignant neoplasms, TRPM8 is aberrantly expressed to variable extents. In the majority of pancreatic adenocarcinoma, TRPM8 is expressed at moderate or high levels, and anti-TRPM8 immunoreactivity positively correlates with the primary tumor size and stage. In the pancreatic adenocarcinoma cell lines that express relatively high levels of TRPM8, short hairpin RNA-mediated interference of TRPM8 expression impaired their ability of invasion. These data suggest that aberrantly expressed TRPM8 channels play contributory roles in pancreatic tumor growth and metastasis, and support exploration of TRPM8 as a biomarker and target of pancreatic adenocarcinoma. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Figures

Open AccessArticle PKC-dependent Phosphorylation of the H1 Histamine Receptor Modulates TRPC6 Activity
Cells 2014, 3(2), 247-257; doi:10.3390/cells3020247
Received: 18 February 2014 / Revised: 17 March 2014 / Accepted: 25 March 2014 / Published: 4 April 2014
Cited by 1 | PDF Full-text (582 KB) | HTML Full-text | XML Full-text
Abstract
Transient receptor potential canonical 6 (TRPC6) is a cation selective, DAG-regulated, Ca2+-permeable channel activated by the agonists of Gq-protein-coupled heptahelical receptors. Dysfunctions of TRPC6 are implicated in the pathogenesis of various cardiovascular and kidney conditions such as vasospasm and
[...] Read more.
Transient receptor potential canonical 6 (TRPC6) is a cation selective, DAG-regulated, Ca2+-permeable channel activated by the agonists of Gq-protein-coupled heptahelical receptors. Dysfunctions of TRPC6 are implicated in the pathogenesis of various cardiovascular and kidney conditions such as vasospasm and glomerulosclerosis. When stimulated by agonists of the histamine H1 receptor (H1R), TRPC6 activity decays to the baseline despite the continuous presence of the agonist. In this study, we examined whether H1R desensitization contributes to regulating the decay rate of TRPC6 activity upon receptor stimulation. We employed the HEK expression system and a biosensor allowing us to simultaneously detect the changes in intracellular diacylglycerol (DAG) and Ca2+ concentrations. We found that the histamine-induced DAG response was biphasic, in which a transient peak was followed by maintained elevated plateau, suggesting that desensitization of H1R takes place in the presence of histamine. The application of PKC inhibitor Gö6983 slowed the decay rate of intracellular DAG concentration. Activation of the mouse H1R mutant lacking a putative PKC phosphorylation site, Ser399, responsible for the receptor desensitization, resulted in a prolonged intracellular DAG increase and greater Mn2+ influx through the TRPC6 channel. Thus, our data support the hypothesis that PKC-dependent H1R phosphorylation leads to a reduced production of intracellular DAG that contributes to TRPC6 activity regulation. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Figures

Review

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Open AccessReview Natural and Synthetic Modulators of the TRPM7 Channel
Cells 2014, 3(4), 1089-1101; doi:10.3390/cells3041089
Received: 26 September 2014 / Revised: 19 November 2014 / Accepted: 20 November 2014 / Published: 27 November 2014
Cited by 6 | PDF Full-text (932 KB) | HTML Full-text | XML Full-text
Abstract
Transient receptor potential cation channel subfamily M member 7 (TRPM7) is a bi-functional protein comprising a TRP ion channel segment linked to an α-type protein kinase domain. Genetic inactivation of TRPM7 revealed its central role in magnesium metabolism, cell motility, proliferation and differentiation.
[...] Read more.
Transient receptor potential cation channel subfamily M member 7 (TRPM7) is a bi-functional protein comprising a TRP ion channel segment linked to an α-type protein kinase domain. Genetic inactivation of TRPM7 revealed its central role in magnesium metabolism, cell motility, proliferation and differentiation. TRPM7 is associated with anoxic neuronal death, cardiac fibrosis and tumor progression highlighting TRPM7 as a new drug target. Recently, several laboratories have independently identified pharmacological compounds inhibiting or activating the TRPM7 channel. The recently found TRPM7 modulators were used as new experimental tools to unravel cellular functions of the TRPM7 channel. Here, we provide a concise overview of this emerging field. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessReview Classical Transient Receptor Potential 1 (TRPC1): Channel or Channel Regulator?
Cells 2014, 3(4), 939-962; doi:10.3390/cells3040939
Received: 8 August 2014 / Revised: 7 September 2014 / Accepted: 18 September 2014 / Published: 29 September 2014
Cited by 10 | PDF Full-text (1788 KB) | HTML Full-text | XML Full-text
Abstract
In contrast to other Classical Transient Receptor Potential TRPC channels the function of TRPC1 as an ion channel is a matter of debate, because it is often difficult to obtain substantial functional signals over background in response to over-expression of TRPC1 alone. Along
[...] Read more.
In contrast to other Classical Transient Receptor Potential TRPC channels the function of TRPC1 as an ion channel is a matter of debate, because it is often difficult to obtain substantial functional signals over background in response to over-expression of TRPC1 alone. Along these lines, heterologously expressed TRPC1 is poorly translocated to the plasma membrane as a homotetramer and may not function on its own physiologically, but may rather be an important linker and regulator protein in heteromeric TRPC channel tetramers. However, due to the lack of specific TRPC1 antibodies able to detect native TRPC1 channels in primary cells, identification of functional TRPC1 containing heteromeric TRPC channel complexes in the plasma membrane is still challenging. Moreover, an extended TRPC1 cDNA, which was recently discovered, may seriously question results obtained in heterologous expression systems transfected with shortened cDNA versions. Therefore, this review will focus on the current status of research on TRPC1 function obtained in primary cells and a TRPC1-deficient mouse model. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Figures

Open AccessReview TRPV1 and Endocannabinoids: Emerging Molecular Signals that Modulate Mammalian Vision
Cells 2014, 3(3), 914-938; doi:10.3390/cells3030914
Received: 1 July 2014 / Revised: 27 August 2014 / Accepted: 5 September 2014 / Published: 12 September 2014
Cited by 6 | PDF Full-text (1231 KB) | HTML Full-text | XML Full-text
Abstract
Transient Receptor Potential Vanilloid 1 (TRPV1) subunits form a polymodal cation channel responsive to capsaicin, heat, acidity and endogenous metabolites of polyunsaturated fatty acids. While originally reported to serve as a pain and heat detector in the peripheral nervous system, TRPV1 has been
[...] Read more.
Transient Receptor Potential Vanilloid 1 (TRPV1) subunits form a polymodal cation channel responsive to capsaicin, heat, acidity and endogenous metabolites of polyunsaturated fatty acids. While originally reported to serve as a pain and heat detector in the peripheral nervous system, TRPV1 has been implicated in the modulation of blood flow and osmoregulation but also neurotransmission, postsynaptic neuronal excitability and synaptic plasticity within the central nervous system. In addition to its central role in nociception, evidence is accumulating that TRPV1 contributes to stimulus transduction and/or processing in other sensory modalities, including thermosensation, mechanotransduction and vision. For example, TRPV1, in conjunction with intrinsic cannabinoid signaling, might contribute to retinal ganglion cell (RGC) axonal transport and excitability, cytokine release from microglial cells and regulation of retinal vasculature. While excessive TRPV1 activity was proposed to induce RGC excitotoxicity, physiological TRPV1 activity might serve a neuroprotective function within the complex context of retinal endocannabinoid signaling. In this review we evaluate the current evidence for localization and function of TRPV1 channels within the mammalian retina and explore the potential interaction of this intriguing nociceptor with endogenous agonists and modulators. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessReview Cellular and Developmental Biology of TRPM7 Channel-Kinase: Implicated Roles in Cancer
Cells 2014, 3(3), 751-777; doi:10.3390/cells3030751
Received: 10 March 2014 / Revised: 15 July 2014 / Accepted: 15 July 2014 / Published: 30 July 2014
Cited by 7 | PDF Full-text (1104 KB) | HTML Full-text | XML Full-text
Abstract
The transient receptor potential melastatin-subfamily member 7 (TRPM7) is a ubiquitously expressed cation-permeable ion channel with intrinsic kinase activity that plays important roles in various physiological functions. Biochemical and electrophysiological studies, in combination with molecular analyses of TRPM7, have generated insights into its
[...] Read more.
The transient receptor potential melastatin-subfamily member 7 (TRPM7) is a ubiquitously expressed cation-permeable ion channel with intrinsic kinase activity that plays important roles in various physiological functions. Biochemical and electrophysiological studies, in combination with molecular analyses of TRPM7, have generated insights into its functions as a cellular sensor and transducer of physicochemical stimuli. Accumulating evidence indicates that TRPM7 channel-kinase is essential for cellular processes, such as proliferation, survival, differentiation, growth, and migration. Experimental studies in model organisms, such as zebrafish, mouse, and frog, have begun to elucidate the pleiotropic roles of TRPM7 during embryonic development from gastrulation to organogenesis. Aberrant expression and/or activity of the TRPM7 channel-kinase have been implicated in human diseases including a variety of cancer. Studying the functional roles of TRPM7 and the underlying mechanisms in normal cells and developmental processes is expected to help understand how TRPM7 channel-kinase contributes to pathogenesis, such as malignant neoplasia. On the other hand, studies of TRPM7 in diseases, particularly cancer, will help shed new light in the normal functions of TRPM7 under physiological conditions. In this article, we will provide an updated review of the structural features and biological functions of TRPM7, present a summary of current knowledge of its roles in development and cancer, and discuss the potential of TRPM7 as a clinical biomarker and therapeutic target in malignant diseases. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Figures

Open AccessReview TRPV Channels in Mast Cells as a Target for Low-Level-Laser Therapy
Cells 2014, 3(3), 662-673; doi:10.3390/cells3030662
Received: 5 May 2014 / Revised: 9 June 2014 / Accepted: 17 June 2014 / Published: 26 June 2014
Cited by 6 | PDF Full-text (409 KB) | HTML Full-text | XML Full-text
Abstract
Low-level laser irradiation in the visible as well as infrared range is applied to skin for treatment of various diseases. Here we summarize and discuss effects of laser irradiation on mast cells that leads to degranulation of the cells. This process may contribute
[...] Read more.
Low-level laser irradiation in the visible as well as infrared range is applied to skin for treatment of various diseases. Here we summarize and discuss effects of laser irradiation on mast cells that leads to degranulation of the cells. This process may contribute to initial steps in the final medical effects. We suggest that activation of TRPV channels in the mast cells forms a basis for the underlying mechanisms and that released ATP and histamine may be putative mediators for therapeutic effects. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessReview TRPV1: A Potential Drug Target for Treating Various Diseases
Cells 2014, 3(2), 517-545; doi:10.3390/cells3020517
Received: 27 March 2014 / Revised: 14 May 2014 / Accepted: 15 May 2014 / Published: 23 May 2014
Cited by 14 | PDF Full-text (657 KB) | HTML Full-text | XML Full-text
Abstract
Transient receptor potential vanilloid 1 (TRPV1) is an ion channel present on sensory neurons which is activated by heat, protons, capsaicin and a variety of endogenous lipids termed endovanilloids. As such, TRPV1 serves as a multimodal sensor of noxious stimuli which could trigger
[...] Read more.
Transient receptor potential vanilloid 1 (TRPV1) is an ion channel present on sensory neurons which is activated by heat, protons, capsaicin and a variety of endogenous lipids termed endovanilloids. As such, TRPV1 serves as a multimodal sensor of noxious stimuli which could trigger counteractive measures to avoid pain and injury. Activation of TRPV1 has been linked to chronic inflammatory pain conditions and peripheral neuropathy, as observed in diabetes. Expression of TRPV1 is also observed in non-neuronal sites such as the epithelium of bladder and lungs and in hair cells of the cochlea. At these sites, activation of TRPV1 has been implicated in the pathophysiology of diseases such as cystitis, asthma and hearing loss. Therefore, drugs which could modulate TRPV1 channel activity could be useful for the treatment of conditions ranging from chronic pain to hearing loss. This review describes the roles of TRPV1 in the normal physiology and pathophysiology of selected organs of the body and highlights how drugs targeting this channel could be important clinically. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessReview Physiological Function and Characterization of TRPCs in Neurons
Cells 2014, 3(2), 455-475; doi:10.3390/cells3020455
Received: 21 March 2014 / Revised: 22 April 2014 / Accepted: 13 May 2014 / Published: 21 May 2014
Cited by 5 | PDF Full-text (387 KB) | HTML Full-text | XML Full-text
Abstract
Ca2+ entry is essential for regulating vital physiological functions in all neuronal cells. Although neurons are engaged in multiple modes of Ca2+ entry that regulates variety of neuronal functions, we will only discuss a subset of specialized Ca2+-permeable non-selective
[...] Read more.
Ca2+ entry is essential for regulating vital physiological functions in all neuronal cells. Although neurons are engaged in multiple modes of Ca2+ entry that regulates variety of neuronal functions, we will only discuss a subset of specialized Ca2+-permeable non-selective Transient Receptor Potential Canonical (TRPC) channels and summarize their physiological and pathological role in these excitable cells. Depletion of endoplasmic reticulum (ER) Ca2+ stores, due to G-protein coupled receptor activation, has been shown to activate TRPC channels in both excitable and non-excitable cells. While all seven members of TRPC channels are predominately expressed in neuronal cells, the ion channel properties, mode of activation, and their physiological responses are quite distinct. Moreover, many of these TRPC channels have also been suggested to be associated with neuronal development, proliferation and differentiation. In addition, TRPCs also regulate neurosecretion, long-term potentiation and synaptic plasticity. Similarly, perturbations in Ca2+ entry via the TRPC channels have been also suggested in a spectrum of neuropathological conditions. Hence, understanding the precise involvement of TRPCs in neuronal function and in neurodegenerative conditions would presumably unveil avenues for plausible therapeutic interventions for these devastating neuronal diseases. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessReview TRP Channels Involved in Spontaneous L-Glutamate Release Enhancement in the Adult Rat Spinal Substantia Gelatinosa
Cells 2014, 3(2), 331-362; doi:10.3390/cells3020331
Received: 28 February 2014 / Revised: 10 April 2014 / Accepted: 18 April 2014 / Published: 29 April 2014
Cited by 9 | PDF Full-text (2462 KB) | HTML Full-text | XML Full-text
Abstract
The spinal substantia gelatinosa (SG) plays a pivotal role in modulating nociceptive transmission through dorsal root ganglion (DRG) neurons from the periphery. TRP channels such as TRPV1 and TRPA1 channels expressed in the SG are involved in the regulation of the nociceptive transmission.
[...] Read more.
The spinal substantia gelatinosa (SG) plays a pivotal role in modulating nociceptive transmission through dorsal root ganglion (DRG) neurons from the periphery. TRP channels such as TRPV1 and TRPA1 channels expressed in the SG are involved in the regulation of the nociceptive transmission. On the other hand, the TRP channels located in the peripheral terminals of the DRG neurons are activated by nociceptive stimuli given to the periphery and also by plant-derived chemicals, which generates a membrane depolarization. The chemicals also activate the TRP channels in the SG. In this review, we introduce how synaptic transmissions in the SG neurons are affected by various plant-derived chemicals and suggest that the peripheral and central TRP channels may differ in property from each other. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessReview The Role of Canonical Transient Receptor Potential Channels in Seizure and Excitotoxicity
Cells 2014, 3(2), 288-303; doi:10.3390/cells3020288
Received: 28 February 2014 / Revised: 29 March 2014 / Accepted: 2 April 2014 / Published: 9 April 2014
Cited by 2 | PDF Full-text (658 KB) | HTML Full-text | XML Full-text
Abstract
Canonical transient receptor potential (TRPC) channels are a family of polymodal cation channels with some degree of Ca2+ permeability. Although initially thought to be channels mediating store-operated Ca2+ influx, TRPC channels can be activated by stimulation of Gq-coupled G-protein coupled receptors,
[...] Read more.
Canonical transient receptor potential (TRPC) channels are a family of polymodal cation channels with some degree of Ca2+ permeability. Although initially thought to be channels mediating store-operated Ca2+ influx, TRPC channels can be activated by stimulation of Gq-coupled G-protein coupled receptors, or by an increase in intracellular free Ca2+ concentration. Thus, activation of TRPC channels could be a common downstream event of many signaling pathways that contribute to seizure and excitotoxicity, such as N-methyl-D-aspartate (NMDA) receptor-mediated Ca2+ influx, or metabotropic glutamate receptor activation. Recent studies with genetic ablation of various TRPC family members have demonstrated that TRPC channels, in particular heteromeric TRPC1/4 channels and homomeric TRPC5 channels, play a critical role in both pilocarpine-induced acute seizures and neuronal cell death. However, exact underlying mechanisms remain to be fully elucidated, and selective TRPC modulators and antibodies with better specificity are urgently needed for future research. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessReview Post-Translational Modifications of TRP Channels
Cells 2014, 3(2), 258-287; doi:10.3390/cells3020258
Received: 28 February 2014 / Revised: 25 March 2014 / Accepted: 27 March 2014 / Published: 8 April 2014
Cited by 4 | PDF Full-text (1325 KB) | HTML Full-text | XML Full-text
Abstract
Transient receptor potential (TRP) channels constitute an ancient family of cation channels that have been found in many eukaryotic organisms from yeast to human. TRP channels exert a multitude of physiological functions ranging from Ca2+ homeostasis in the kidney to pain reception
[...] Read more.
Transient receptor potential (TRP) channels constitute an ancient family of cation channels that have been found in many eukaryotic organisms from yeast to human. TRP channels exert a multitude of physiological functions ranging from Ca2+ homeostasis in the kidney to pain reception and vision. These channels are activated by a wide range of stimuli and undergo covalent post-translational modifications that affect and modulate their subcellular targeting, their biophysical properties, or channel gating. These modifications include N-linked glycosylation, protein phosphorylation, and covalent attachment of chemicals that reversibly bind to specific cysteine residues. The latter modification represents an unusual activation mechanism of ligand-gated ion channels that is in contrast to the lock-and-key paradigm of receptor activation by its agonists. In this review, we summarize the post-translational modifications identified on TRP channels and, when available, explain their physiological role. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessReview Loss of TRPV2 Homeostatic Control of Cell Proliferation Drives Tumor Progression
Cells 2014, 3(1), 112-128; doi:10.3390/cells3010112
Received: 19 December 2013 / Revised: 22 January 2014 / Accepted: 8 February 2014 / Published: 19 February 2014
Cited by 3 | PDF Full-text (297 KB) | HTML Full-text | XML Full-text | Correction
Abstract
Herein we evaluate the involvement of the TRPV2 channel, belonging to the Transient Receptor Potential Vanilloid channel family (TRPVs), in development and progression of different tumor types. In normal cells, the activation of TRPV2 channels by growth factors, hormones, and endocannabinoids induces a
[...] Read more.
Herein we evaluate the involvement of the TRPV2 channel, belonging to the Transient Receptor Potential Vanilloid channel family (TRPVs), in development and progression of different tumor types. In normal cells, the activation of TRPV2 channels by growth factors, hormones, and endocannabinoids induces a translocation of the receptor from the endosomal compartment to the plasma membrane, which results in abrogation of cell proliferation and induction of cell death. Consequently, loss or inactivation of TRPV2 signaling (e.g., glioblastomas), induces unchecked proliferation, resistance to apoptotic signals and increased resistance to CD95-induced apoptotic cell death. On the other hand, in prostate cancer cells, Ca2+-dependent activation of TRPV2 induced by lysophospholipids increases the invasion of tumor cells. In addition, the progression of prostate cancer to the castration-resistant phenotype is characterized by de novo TRPV2 expression, with higher TRPV2 transcript levels in patients with metastatic cancer. Finally, TRPV2 functional expression in tumor cells can also depend on the presence of alternative splice variants of TRPV2 mRNA that act as dominant-negative mutant of wild-type TRPV2 channels, by inhibiting its trafficking and translocation to the plasma membrane. In conclusion, as TRP channels are altered in human cancers, and their blockage impair tumor progression, they appear to be a very promising targets for early diagnosis and chemotherapy. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)

Other

Jump to: Research, Review

Open AccessCorrection Correction: Sadofsky, L.R., et al. Unique Responses are Observed in Transient Receptor Potential Ankyrin 1 and Vanilloid 1 (TRPA1 and TRPV1) Co-Expressing Cells. Cells 2014, 3, 616-626
Cells 2014, 3(4), 994-995; doi:10.3390/cells3040994
Received: 3 September 2014 / Accepted: 4 September 2014 / Published: 27 October 2014
PDF Full-text (594 KB) | HTML Full-text | XML Full-text
Abstract
The authors wish to make the following corrections to this paper [1]: In Table 2 on page 623, the Quercinitol activation value for TRPA1V1 should be 2.3 instead of 57.6. Quercinitol does not activate TRPA1V1. We thank Michael J.M. Fisher (University of Erlangen,
[...] Read more.
The authors wish to make the following corrections to this paper [1]: In Table 2 on page 623, the Quercinitol activation value for TRPA1V1 should be 2.3 instead of 57.6. Quercinitol does not activate TRPA1V1. We thank Michael J.M. Fisher (University of Erlangen, Germany) for his feedback which helped us to review our result. The authors would like to apologize for any inconvenience caused to the readers by these changes. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessCorrection Correction: Liberati, S., et al. Loss of TRPV2 Homeostatic Control of Cell Proliferation Drives Tumor Progression. Cells 2014, 3, 112–128
Cells 2014, 3(2), 660-661; doi:10.3390/cells3020660
Received: 12 June 2014 / Accepted: 16 June 2014 / Published: 20 June 2014
PDF Full-text (113 KB) | HTML Full-text | XML Full-text
Abstract The authors wish to make the following corrections to this paper [1]: [...] Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)

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