scholarly journals TRPC Channels in the SOCE Scenario

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 126 ◽  
Author(s):  
Jose J. Lopez ◽  
Isaac Jardin ◽  
Jose Sanchez-Collado ◽  
Ginés M. Salido ◽  
Tarik Smani ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Cell Types ◽  
Trpc Channels ◽  
Crac Channels ◽  
Relevant Role ◽  
Transient Receptor ◽  
Trpc Proteins ◽  
Soc Channels

Transient receptor potential (TRP) proteins form non-selective Ca2+ permeable channels that contribute to the modulation of a number of physiological functions in a variety of cell types. Since the identification of TRP proteins in Drosophila, it is well known that these channels are activated by stimuli that induce PIP2 hydrolysis. The canonical TRP (TRPC) channels have long been suggested to be constituents of the store-operated Ca2+ (SOC) channels; however, none of the TRPC channels generate Ca2+ currents that resemble ICRAC. STIM1 and Orai1 have been identified as the components of the Ca2+ release-activated Ca2+ (CRAC) channels and there is a body of evidence supporting that STIM1 is able to gate Orai1 and TRPC1 in order to mediate non-selective cation currents named ISOC. STIM1 has been found to interact to and activate Orai1 and TRPC1 by different mechanisms and the involvement of TRPC1 in store-operated Ca2+ entry requires both STIM1 and Orai1. In addition to the participation of TRPC1 in the ISOC currents, TRPC1 and other TRPC proteins might play a relevant role modulating Orai1 channel function. This review summarizes the functional role of TRPC channels in the STIM1–Orai1 scenario.

Expression and relative abundance of short transient receptor potential channels in the rat renal microcirculation

2004 ◽  
Vol 286 (3) ◽  
pp. F546-F551 ◽  
Author(s):  
Carie S. Facemire ◽  
Peter J. Mohler ◽  
William J. Arendshorst
Keyword(s):  
Relative Abundance ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Cell Types ◽  
Calcium Entry ◽  
Transient Receptor Potential Channels ◽  
Trpc Channels ◽  
Renal Microcirculation ◽  
Resistance Vessels ◽  
Transient Receptor

In the resistance vessels of the renal microcirculation, store- and/or receptor-operated calcium entry contribute to the rise in vascular smooth muscle cell (VSMC) intracellular calcium concentration in response to vasoconstrictor hormones. Short transient receptor potential (TRPC) channels are widely expressed in mammalian tissues and are proposed mediators of voltage-independent cation entry in multiple cell types, including VSMCs. The seven members of the TRPC gene family (TRPC1-7) encode subunit proteins that are thought to form homo- and heterotetrameric channels that are differentially regulated depending on their subunit composition. In the present study, we demonstrate the relative abundance of TRPC mRNA and protein in freshly isolated rat renal resistance vessels, glomeruli, and aorta. TRPC1, 3, 4, 5, and 6 mRNA and protein were detected in both renal resistance vessels and aorta, whereas TRPC2 and TRPC7 mRNA were not expressed. TRPC1, 3, 5, and 6 protein was present in glomeruli. TRPC3 and TRPC6 protein levels were significantly greater in the renal resistance vessels, about six- to eightfold higher than in aorta. These data suggest that TRPC3 and TRPC6 may play a role in mediating voltage-independent calcium entry in renal resistance vessels that is functionally distinct from that in aorta.

scholarly journals TRPC6 channels and their binding partners in podocytes: role in glomerular filtration and pathophysiology

2010 ◽  
Vol 299 (4) ◽  
pp. F689-F701 ◽  
Author(s):  
Stuart E. Dryer ◽  
Jochen Reiser
Keyword(s):  
Cell Biology ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Glomerular Disease ◽  
Slit Diaphragm ◽  
Trpc Channels ◽  
Structural Elements ◽  
Signaling Dynamics ◽  
Transient Receptor

Loss or dysfunction of podocytes is a major cause of glomerular kidney disease. Several genetic forms of glomerular disease are caused by mutations in genes that encode structural elements of the slit diaphragm or the underlying cytoskeleton of podocyte foot processes. The recent discovery that gain-of-function mutations in Ca2+-permeable canonical transient receptor potential-6 channels (TRPC6) underlie a subset of familial forms of focal segmental glomerulosclerosis (FSGS) has focused attention on the basic cellular physiology of podocytes. Several recent studies have examined the role of Ca2+ dynamics in normal podocyte function and their possible contributions to glomerular disease. This review summarizes the properties of TRPC6 and related channels, focusing on their permeation and gating properties, the nature of mutations associated with familial FSGS, and the role of TRPC channels in podocyte cell biology as well as in glomerular pathophysiology. TRPC6 interacts with several proteins in podocytes, including essential slit diaphragm proteins and mechanosensitive large-conductance Ca2+-activated K+ channels. The signaling dynamics controlling ion channel function and localization in podocytes appear to be quite complex.

Pharmacology of TRPC Channels and Its Potential in Cardiovascular and Metabolic Medicine

2021 ◽  
Vol 62 (1) ◽  
Author(s):  
Robin S. Bon ◽  
David J. Wright ◽  
David J. Beech ◽  
Piruthivi Sukumar
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Annual Review ◽  
Publication Date ◽  
Trpc Channels ◽  
Trpc Channel ◽  
Channel Inhibition ◽  
Transient Receptor ◽  
Physical And Chemical ◽  
Trpc Proteins

Transient receptor potential canonical (TRPC) proteins assemble to form homo- or heterotetrameric, nonselective cation channels permeable to K+, Na+, and Ca2+. TRPC channels are thought to act as complex integrators of physical and chemical environmental stimuli. Although the understanding of essential physiological roles of TRPC channels is incomplete, their implication in various pathological mechanisms and conditions of the nervous system, kidneys, and cardiovascular system in combination with the lack of major adverse effects of TRPC knockout or TRPC channel inhibition is driving the search of TRPC channel modulators as potential therapeutics. Here, we review the most promising small-molecule TRPC channel modulators, the understanding of their mode of action, and their potential in the study and treatment of cardiovascular and metabolic disease. Expected final online publication date for the Annual Review of Pharmacology and Toxicology, Volume 62 is January 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

SARAF modulates TRPC1, but not TRPC6, channel function in a STIM1-independent manner

2016 ◽  
Vol 473 (20) ◽  
pp. 3581-3595 ◽  
Author(s):  
Letizia Albarrán ◽  
José J. López ◽  
Luis J. Gómez ◽  
Ginés M. Salido ◽  
Juan A. Rosado
Keyword(s):  
Transient Receptor Potential ◽  
Cell Function ◽  
Receptor Potential ◽  
Independent Manner ◽  
Channel Function ◽  
Relevant Role ◽  
Trpc6 Channel ◽  
Transient Receptor ◽  
Trpc1 Channel

Canonical transient receptor potential-1 (TRPC1) is an almost ubiquitously expressed channel that plays a relevant role in cell function. As other TRPC members, TRPC1 forms receptor-operated cation channels that exhibit both STIM1-dependent and store-independent behaviour. The STIM1 inhibitor SARAF (for store-operated Ca2+ entry (SOCE)-associated regulatory factor) modulates SOCE by interaction with the STIM1 region responsible for Orai1 activation (SOAR). Furthermore, SARAF modulates Ca2+ entry through the arachidonate-regulated Ca2+ (ARC) channels, consisting of Orai1 and Orai3 heteropentamers and plasma membrane-resident STIM1. While a role for STIM1–Orai1-mediated signals has been demonstrated, the possible role of SARAF in TRPC1 function remains unknown. Here, we provide evidence for the interaction of SARAF with TRPC1, independently of STIM1 both in STIM1-deficient NG115-401L cells and SH-SY5Y cells endogenously expressing STIM1. Silencing of SARAF expression in STIM1-deficient cells demonstrated that SARAF plays a negative regulatory role in TRPC1-mediated Ca2+ entry. The interaction of SARAF with TRPC1 in STIM1-deficient cells, as well as with the TRPC1 pool not associated with STIM1 in STIM1-expressing cells was enhanced by stimulation with the physiological agonist ATP. In contrast with TRPC1, we found that the interaction between SARAF and TRPC6 was constitutive rather than inducible by agonist stimulation. Furthermore, we found that SARAF expression silencing was without effect on Ca2+ entry evoked by agonists in TRPC6 overexpressing cells, as well as in Ca2+ influx evoked by the TRPC6 activator Hyp9. These findings provide evidence for a new regulator of TRPC1 channel function and highlight the relevance of SARAF in intracellular Ca2+ homeostasis.

scholarly journals Contemporary views on inflammatory pain mechanisms: TRPing over innate and microglial pathways

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2425 ◽  
Author(s):  
Zhonghui Guan ◽  
Judith Hellman ◽  
Mark Schumacher
Keyword(s):  
Cellular Response ◽  
Transient Receptor Potential ◽  
Tissue Injury ◽  
Trauma Surgery ◽  
Receptor Potential ◽  
Cell Types ◽  
Metabolic Dysfunction ◽  
Pain Mechanisms ◽  
Transient Receptor

Tissue injury, whether by trauma, surgical intervention, metabolic dysfunction, ischemia, or infection, evokes a complex cellular response (inflammation) that is associated with painful hyperalgesic states. Although in the acute stages it is necessary for protective reflexes and wound healing, inflammation may persist well beyond the need for tissue repair or survival. Prolonged inflammation may well represent the greatest challenge mammalian organisms face, as it can lead to chronic painful conditions, organ dysfunction, morbidity, and death. The complexity of the inflammatory response reflects not only the inciting event (infection, trauma, surgery, cancer, or autoimmune) but also the involvement of heterogeneous cell types including neuronal (primary afferents, sensory ganglion, and spinal cord), non-neuronal (endothelial, keratinocytes, epithelial, and fibroblasts), and immune cells. In this commentary, we will examine 1.) the expression and regulation of two members of the transient receptor potential family in primary afferent nociceptors and their activation/regulation by products of inflammation, 2.) the role of innate immune pathways that drive inflammation, and 3.) the central nervous system’s response to injury with a focus on the activation of spinal microglia driving painful hyperalgesic states.

scholarly journals How TRPC Channels Modulate Hippocampal Function

2020 ◽  
Vol 21 (11) ◽  
pp. 3915
Author(s):  
Roberta Gualdani ◽  
Philippe Gailly
Keyword(s):  
Transient Receptor Potential ◽  
Neuronal Excitability ◽  
Receptor Potential ◽  
Trpc Channels ◽  
Persistent Activity ◽  
Hippocampal Function ◽  
Different Types ◽  
Transient Receptor ◽  
Neuronal Functions ◽  
Trpc Proteins

Transient receptor potential canonical (TRPC) proteins constitute a group of receptor-operated calcium-permeable nonselective cationic membrane channels of the TRP superfamily. They are largely expressed in the hippocampus and are able to modulate neuronal functions. Accordingly, they have been involved in different hippocampal functions such as learning processes and different types of memories, as well as hippocampal dysfunctions such as seizures. This review covers the mechanisms of activation of these channels, how these channels can modulate neuronal excitability, in particular the after-burst hyperpolarization, and in the persistent activity, how they control synaptic plasticity including pre- and postsynaptic processes and how they can interfere with cell survival and neurogenesis.

TRPC channels in vascular cell function

2010 ◽  
Vol 103 (02) ◽  
pp. 262-270 ◽  
Author(s):  
Thomas Gudermann ◽  
Alexander Dietrich ◽  
Hermann Kalwa
Keyword(s):  
Common Property ◽  
Transient Receptor Potential ◽  
Cell Function ◽  
Vascular System ◽  
Receptor Potential ◽  
Trpc Channels ◽  
The Common ◽  
Transient Receptor ◽  
Isolated Tissues ◽  
Trpc Proteins

SummaryThe mammalian transient receptor potential (TRP) superfamily of non-selective cation channels can be divided into six major families. Among them, the “classical” or “canonical” TRPC family is most closely related to Drosophila TRP, the founding member of the superfamily. All seven channels of this family designated TRPC1–7 share the common property of receptor-operated activation through phospholipase C (PLC)-coupled receptors, but their regulation by store-dependent mechanisms involving the proteins STIM and ORAi is still discussed controversially. This review will focus on the proposed functions of TRPC proteins in cells of the vascular system (e.g. platelets, smooth muscle cells and endothelial cells) and will present data concerning their physiological functions analysed in isolated tissues with down-regulated channel activity and in gene-deficient mouse models.

scholarly journals Interactions between Chemesthesis and Taste: Role of TRPA1 and TRPV1

2021 ◽  
Vol 22 (7) ◽  
pp. 3360
Author(s):  
Mee-Ra Rhyu ◽  
Yiseul Kim ◽  
Vijay Lyall
Keyword(s):  
Transient Receptor Potential ◽  
Taste Receptor ◽  
Sensory Nerve ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Trpv1 Channels ◽  
Trigeminal Neurons ◽  
Calcitonin Gene ◽  
Transient Receptor

In addition to the sense of taste and olfaction, chemesthesis, the sensation of irritation, pungency, cooling, warmth, or burning elicited by spices and herbs, plays a central role in food consumption. Many plant-derived molecules demonstrate their chemesthetic properties via the opening of transient receptor potential ankyrin 1 (TRPA1) and transient receptor potential vanilloid 1 (TRPV1) channels. TRPA1 and TRPV1 are structurally related thermosensitive cation channels and are often co-expressed in sensory nerve endings. TRPA1 and TRPV1 can also indirectly influence some, but not all, primary taste qualities via the release of substance P and calcitonin gene-related peptide (CGRP) from trigeminal neurons and their subsequent effects on CGRP receptor expressed in Type III taste receptor cells. Here, we will review the effect of some chemesthetic agonists of TRPA1 and TRPV1 and their influence on bitter, sour, and salt taste qualities.

Sign in / Sign up

Export Citation Format

Share Document