Permeation, Regulation and Control of Expression of TRP Channels by Trace Metal Ions
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A Computational Model of Large Conductance Voltage and Calcium
Journal of Computational Neuroscience (2019) 46:233–256 https://doi.org/10.1007/s10827-019-00713-9 A computational model of large conductance voltage and calcium activated potassium channels: implications for calcium dynamics and electrophysiology in detrusor smooth muscle cells Suranjana Gupta1 · Rohit Manchanda1 Received: 11 September 2018 / Revised: 14 February 2019 / Accepted: 19 February 2019 / Published online: 25 April 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract The large conductance voltage and calcium activated potassium (BK) channels play a crucial role in regulating the excitability of detrusor smooth muscle, which lines the wall of the urinary bladder. These channels have been widely characterized in terms of their molecular structure, pharmacology and electrophysiology. They control the repolarising and hyperpolarising phases of the action potential, thereby regulating the firing frequency and contraction profiles of the smooth muscle. Several groups have reported varied profiles of BK currents and I-V curves under similar experimental conditions. However, no single computational model has been able to reconcile these apparent discrepancies. In view of the channels’ physiological importance, it is imperative to understand their mechanistic underpinnings so that a realistic model can be created. This paper presents a computational model of the BK channel, based on the Hodgkin-Huxley formalism, constructed by utilising three activation processes — membrane potential, calcium inflow from voltage-gated calcium channels on the membrane and calcium released from the ryanodine receptors present on the sarcoplasmic reticulum. In our model, we attribute the discrepant profiles to the underlying cytosolic calcium received by the channel during its activation. The model enables us to make heuristic predictions regarding the nature of the sub-membrane calcium dynamics underlying the BK channel’s activation. -
The Role of Transient Receptor Potential Cation Channels in Ca2þ Signaling
Downloaded from http://cshperspectives.cshlp.org/ on October 7, 2021 - Published by Cold Spring Harbor Laboratory Press The Role of Transient Receptor Potential Cation Channels in Ca2þ Signaling Maarten Gees, Barbara Colsoul, and Bernd Nilius KU Leuven, Department of Molecular Cell Biology, Laboratory Ion Channel Research, Campus Gasthuisberg, Herestraat 49, bus 802, Leuven, Belgium Correspondence: [email protected] The 28 mammalian members of the super-family of transient receptor potential (TRP) channels are cation channels, mostly permeable to both monovalent and divalent cations, and can be subdivided into six main subfamilies: the TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPP (polycystin), TRPML (mucolipin), and the TRPA (ankyrin) groups. TRP channels are widely expressed in a large number of different tissues and cell types, and their biological roles appear to be equally diverse. In general, considered as poly- modal cell sensors, they play a much more diverse role than anticipated. Functionally, TRP channels, when activated, cause cell depolarization, which may trigger a plethora of voltage-dependent ion channels. Upon stimulation, Ca2þ permeable TRP channels 2þ 2þ 2þ generate changes in the intracellular Ca concentration, [Ca ]i,byCa entry via the plasma membrane. However, more and more evidence is arising that TRP channels are also located in intracellular organelles and serve as intracellular Ca2þ release channels. This review focuses on three major tasks of TRP channels: (1) the function of TRP channels as Ca2þ entry channels; (2) the electrogenic actions of TRPs; and (3) TRPs as Ca2þ release channels in intracellular organelles. ransient receptor potential (TRP) channels choanoflagellates, yeast, and fungi are primary Tconstitute a large and functionally versatile chemo-, thermo-, or mechanosensors (Cai 2008; family of cation-conducting channel proteins, Wheeler and Brownlee 2008; Chang et al. -
The Intracellular Ca2+ Release Channel TRPML1 Regulates Lower Urinary Tract Smooth Muscle Contractility
The intracellular Ca2+ release channel TRPML1 regulates lower urinary tract smooth muscle contractility Caoimhin S. Griffina, Michael G. Alvaradoa, Evan Yamasakia, Bernard T. Drummb,c, Vivek Krishnana, Sher Alia, Eleanor M. Naglea, Kenton M. Sandersb, and Scott Earleya,1 aDepartment of Pharmacology, Center for Molecular and Cellular Signaling in the Cardiovascular System, Reno School of Medicine, University of Nevada, Reno, NV 89557-0318; bDepartment of Physiology and Cell Biology, Reno School of Medicine, University of Nevada, Reno, NV 89557-0318; and cDepartment of Life & Health Sciences, Dundalk Institute of Technology, Louth, Ireland A91 K584 Edited by Mark T. Nelson, University of Vermont, Burlington, VT, and approved October 13, 2020 (received for review August 12, 2020) TRPML1 (transient receptor potential mucolipin 1) is a Ca2+-perme- including dense granulomembranous storage bodies in neurons, able, nonselective cation channel that is predominantly localized to elevated plasma gastrin, vacuolization in the gastric mucosa, and the membranes of late endosomes and lysosomes (LELs). Intracellular retinal degeneration (14). Interestingly, however, an anatomical release of Ca2+ through TRPML1 is thought to be pivotal for mainte- examination of these mice reveals dramatically distended bladders nance of intravesicular acidic pH as well as the maturation, fusion, and (14), leading us to question how TRPML1, an intracellular Ca2+-re- trafficking of LELs. Interestingly, genetic ablation of TRPML1 in mice lease channel important in LEL function, affects bladder physiology. −/− (Mcoln1 ) induces a hyperdistended/hypertrophic bladder phenotype. The lower urinary tract (LUT) is composed of the urinary Here, we investigated this phenomenon further by exploring an un- bladder and urethra—structures that serve the simple, reciprocal conventional role for TRPML1 channels in the regulation of Ca2+-signal- functions of storing and voiding urine (15). -
The Intracellular Ca2+ Release Channel TRPML1 Regulates Lower Urinary Tract Smooth Muscle Contractility
The intracellular Ca2+ release channel TRPML1 regulates lower urinary tract smooth muscle contractility Caoimhin S. Griffina, Michael G. Alvaradoa, Evan Yamasakia, Bernard T. Drummb,c, Vivek Krishnana, Sher Alia, Eleanor M. Naglea, Kenton M. Sandersb, and Scott Earleya,1 aDepartment of Pharmacology, Center for Molecular and Cellular Signaling in the Cardiovascular System, Reno School of Medicine, University of Nevada, Reno, NV 89557-0318; bDepartment of Physiology and Cell Biology, Reno School of Medicine, University of Nevada, Reno, NV 89557-0318; and cDepartment of Life & Health Sciences, Dundalk Institute of Technology, Louth, Ireland A91 K584 Edited by Mark T. Nelson, University of Vermont, Burlington, VT, and approved October 13, 2020 (received for review August 12, 2020) TRPML1 (transient receptor potential mucolipin 1) is a Ca2+-perme- including dense granulomembranous storage bodies in neurons, able, nonselective cation channel that is predominantly localized to elevated plasma gastrin, vacuolization in the gastric mucosa, and the membranes of late endosomes and lysosomes (LELs). Intracellular retinal degeneration (14). Interestingly, however, an anatomical release of Ca2+ through TRPML1 is thought to be pivotal for mainte- examination of these mice reveals dramatically distended bladders nance of intravesicular acidic pH as well as the maturation, fusion, and (14), leading us to question how TRPML1, an intracellular Ca2+- trafficking of LELs. Interestingly, genetic ablation of TRPML1 in mice release channel important in LEL function, affects bladder −/− (Mcoln1 ) induces a hyperdistended/hypertrophic bladder phenotype. physiology. Here, we investigated this phenomenon further by exploring an un- The lower urinary tract (LUT) is composed of the urinary conventional role for TRPML1 channels in the regulation of Ca2+-signal- bladder and urethra—structures that serve the simple, reciprocal ing activity and contractility in bladder and urethral smooth muscle cells functions of storing and voiding urine (15). -
Trpc, Trpv and Vascular Disease | Encyclopedia
TRPC, TRPV and Vascular Disease Subjects: Biochemistry Submitted by: Tarik Smani Hajami Definition Ion channels play an important role in vascular function and pathology. In this review we gave an overview of recent findings and discussed the role of TRPC and TRPV channels as major regulators of cellular remodeling and consequent vascular disorders. Here, we focused on their implication in 4 relevant vascular diseases: systemic and pulmonary artery hypertension, atherosclerosis and restenosis. Transient receptor potentials (TRPs) are non-selective cation channels that are widely expressed in vascular beds. They contribute to the Ca2+ influx evoked by a wide spectrum of chemical and physical stimuli, both in endothelial and vascular smooth muscle cells. Within the superfamily of TRP channels, different isoforms of TRPC (canonical) and TRPV (vanilloid) have emerged as important regulators of vascular tone and blood flow pressure. Additionally, several lines of evidence derived from animal models, and even from human subjects, highlighted the role of TRPC and TRPV in vascular remodeling and disease. Dysregulation in the function and/or expression of TRPC and TRPV isoforms likely regulates vascular smooth muscle cells switching from a contractile to a synthetic phenotype. This process contributes to the development and progression of vascular disorders, such as systemic and pulmonary arterial hypertension, atherosclerosis and restenosis. 1. Introduction Blood vessels are composed essentially of two interacting cell types: endothelial cells (ECs) from the tunica intima lining of the vessel wall and vascular smooth muscle cells (VSMCs) from tunica media of the vascular tube. Blood vessels are a complex network, and they differ according to the tissue to which they belong, having diverse cell expressions, structures and functions [1][2][3]. -
Recessive Mutations of the Gene TRPM1 Abrogate on Bipolar Cell Function and Cause Complete Congenital Stationary Night Blindness in Humans
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector REPORT Recessive Mutations of the Gene TRPM1 Abrogate ON Bipolar Cell Function and Cause Complete Congenital Stationary Night Blindness in Humans Zheng Li,1 Panagiotis I. Sergouniotis,1 Michel Michaelides,1,2 Donna S. Mackay,1 Genevieve A. Wright,2 Sophie Devery,2 Anthony T. Moore,1,2 Graham E. Holder,1,2 Anthony G. Robson,1,2 and Andrew R. Webster1,2,* Complete congenital stationary night blindness (cCSNB) is associated with loss of function of rod and cone ON bipolar cells in the mammalian retina. In humans, mutations in NYX and GRM6 have been shown to cause the condition. Through the analysis of a consan- guineous family and screening of nine additional pedigrees, we have identified three families with recessive mutations in the gene TRPM1 encoding transient receptor potential cation channel, subfamily M, member 1, also known as melastatin. A number of other variants of unknown significance were found. All patients had myopia, reduced central vision, nystagmus, and electroretinographic evidence of ON bipolar cell dysfunction. None had abnormalities of skin pigmentation, although other skin conditions were reported. RNA derived from human retina and skin was analyzed and alternate 50 exons were determined. The most 50 exon is likely to harbor an initiation codon, and the protein sequence is highly conserved across vertebrate species. These findings suggest an important role of this specific cation channel for the normal function of ON bipolar cells in the human retina. Congenital stationary night blindness (CSNB) is a group of of the gene encoding transient receptor potential cation genetically determined, nondegenerative disorders of the channel, subfamily M, member 1 (TRPM1 [MIM *603576]) retina associated with lifelong deficient vision in the dark has been discovered in the skin and retina of horses homo- and often nystagmus and myopia. -
Entropy-Based Regulation of Cluster Ion Channel Density
www.nature.com/scientificreports OPEN Molecular and cellular correlates in Kv channel clustering: entropy‑based regulation of cluster ion channel density Limor Lewin1, Esraa Nsasra1, Ella Golbary1, Uzi Hadad2, Irit Orr1 & Ofer Yifrach1* Scafold protein-mediated ion channel clustering at unique membrane sites is important for electrical signaling. Yet, the mechanism(s) by which scafold protein-ion channel interactions lead to channel clustering or how cluster ion channel density is regulated is mostly not known. The voltage‑activated potassium channel (Kv) represents an excellent model to address these questions as the mechanism underlying its interaction with the post-synaptic density 95 (PSD-95) scafold protein is known to be controlled by the length of the extended ‘ball and chain’ sequence comprising the C-terminal channel region. Here, using sub-difraction high-resolution imaging microscopy, we show that Kv channel ‘chain’ length regulates Kv channel density with a ‘bell’-shaped dependence, refecting a balance between thermodynamic considerations controlling ‘chain’ recruitment by PSD-95 and steric hindrance due to the spatial proximity of multiple channel molecules. Our results thus reveal an entropy‑based mode of channel cluster density regulation that mirrors the entropy‑based regulation of the Kv channel-PSD-95 interaction. The implications of these fndings for electrical signaling are discussed. Action potential generation, propagation and the evoked synaptic potential all rely on precisely timed events associated with activation and inactivation gating transitions of voltage-dependent Na + and K + channels, clus- tered in multiple copies at unique membrane sites, such as the initial segment of an axon, nodes of Ranvier, pre-synaptic terminals or at the post-synaptic density (PSD)1–3. -
Transient Receptor Potential (TRP) Channels in Haematological Malignancies: an Update
biomolecules Review Transient Receptor Potential (TRP) Channels in Haematological Malignancies: An Update Federica Maggi 1,2 , Maria Beatrice Morelli 2 , Massimo Nabissi 2 , Oliviero Marinelli 2 , Laura Zeppa 2, Cristina Aguzzi 2, Giorgio Santoni 2 and Consuelo Amantini 3,* 1 Department of Molecular Medicine, Sapienza University, 00185 Rome, Italy; [email protected] 2 Immunopathology Laboratory, School of Pharmacy, University of Camerino, 62032 Camerino, Italy; [email protected] (M.B.M.); [email protected] (M.N.); [email protected] (O.M.); [email protected] (L.Z.); [email protected] (C.A.); [email protected] (G.S.) 3 Immunopathology Laboratory, School of Biosciences and Veterinary Medicine, University of Camerino, 62032 Camerino, Italy * Correspondence: [email protected]; Tel.: +30-0737403312 Abstract: Transient receptor potential (TRP) channels are improving their importance in differ- ent cancers, becoming suitable as promising candidates for precision medicine. Their important contribution in calcium trafficking inside and outside cells is coming to light from many papers published so far. Encouraging results on the correlation between TRP and overall survival (OS) and progression-free survival (PFS) in cancer patients are available, and there are as many promising data from in vitro studies. For what concerns haematological malignancy, the role of TRPs is still not elucidated, and data regarding TRP channel expression have demonstrated great variability throughout blood cancer so far. Thus, the aim of this review is to highlight the most recent findings Citation: Maggi, F.; Morelli, M.B.; on TRP channels in leukaemia and lymphoma, demonstrating their important contribution in the Nabissi, M.; Marinelli, O.; Zeppa, L.; perspective of personalised therapies. -
TRPC5 Regulates Axonal Outgrowth in Developing Retinal Ganglion Cells
Laboratory Investigation (2020) 100:297–310 https://doi.org/10.1038/s41374-019-0347-1 ARTICLE TRPC5 regulates axonal outgrowth in developing retinal ganglion cells 1 1 2 1 1 Mai Oda ● Hanako Yamamoto ● Hidetaka Matsumoto ● Yasuki Ishizaki ● Koji Shibasaki Received: 22 July 2019 / Revised: 15 November 2019 / Accepted: 15 November 2019 / Published online: 16 December 2019 © The Author(s), under exclusive licence to United States and Canadian Academy of Pathology 2019 Abstract The TRPC5 ion channel is activated upon depletion of intracellular calcium stores, as well as by various stimuli such as nitric oxide (NO), membrane stretch, and cold temperatures. TRPC5 is abundantly expressed in the central nervous system where it has important neuronal functions. In the chick retina, TRPC5 expression was shown to be restricted to amacrine cells (ACs) and Müller glial cells, although its expression was also observed in the ganglion cell layer (GCL) in displaced ACs, as determined by their characteristic cell morphology. However, it is possible that this expression analysis alone might be insufficient to fully understand the expression of TRPC5 in retinal ganglion cells (RGCs). Hence, we analyzed TRPC5 expression by in situ hybridization and immunostaining in the developing mouse retina, and for the first time identified that 1234567890();,: 1234567890();,: developing and mature RGCs strongly express TRPC5. The expression begins at E14.5, and is restricted to ACs and RGCs. It was reported that TRPC5 negatively regulates axonal outgrowth in hippocampal neurons. We thus hypothesized that TRPC5 might have similar functions in RGCs since they extend very long axons toward the brain, and this characteristic significantly differs from other retinal cell types. -
TRPC1 Regulates the Activity of a Voltage-Dependent Nonselective Cation Current in Hippocampal CA1 Neurons
cells Article TRPC1 Regulates the Activity of a Voltage-Dependent Nonselective Cation Current in Hippocampal CA1 Neurons 1, 1 1,2 1,3, Frauke Kepura y, Eva Braun , Alexander Dietrich and Tim D. Plant * 1 Pharmakologisches Institut, BPC-Marburg, Fachbereich Medizin, Philipps-Universität Marburg, Karl-von-Frisch-Straße 2, 35043 Marburg, Germany; [email protected] (F.K.); braune@staff.uni-marburg.de (E.B.); [email protected] (A.D.) 2 Walther-Straub-Institut für Pharmakologie und Toxikologie, Ludwig-Maximilians-Universität München, 80336 München, Germany 3 Center for Mind, Brain and Behavior, Philipps-Universität Marburg, 35032 Marburg, Germany * Correspondence: plant@staff.uni-marburg.de; Tel.: +49-6421-28-65038 Present address: Institut für Bodenkunde und Pflanzenernährung/Institut für angewandte Ökologie, y Hochschule Geisenheim University, Von-Lade-Str. 1, 65366 Geisenheim, Germany. Received: 27 November 2019; Accepted: 14 February 2020; Published: 18 February 2020 Abstract: The cation channel subunit TRPC1 is strongly expressed in central neurons including neurons in the CA1 region of the hippocampus where it forms complexes with TRPC4 and TRPC5. To investigate the functional role of TRPC1 in these neurons and in channel function, we compared current responses to group I metabotropic glutamate receptor (mGluR I) activation and looked +/+ / for major differences in dendritic morphology in neurons from TRPC1 and TRPC1− − mice. mGluR I stimulation resulted in the activation of a voltage-dependent nonselective cation current in both genotypes. Deletion of TRPC1 resulted in a modification of the shape of the current-voltage relationship, leading to an inward current increase. In current clamp recordings, the percentage of neurons that responded to depolarization in the presence of an mGluR I agonist with a plateau / potential was increased in TRPC1− − mice. -
Structure of the Mouse TRPC4 Ion Channel 1 2 Jingjing
bioRxiv preprint doi: https://doi.org/10.1101/282715; this version posted March 15, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Structure of the mouse TRPC4 ion channel 2 3 Jingjing Duan1,2*, Jian Li1,3*, Bo Zeng4*, Gui-Lan Chen4, Xiaogang Peng5, Yixing Zhang1, 4 Jianbin Wang1, David E. Clapham2, Zongli Li6#, Jin Zhang1# 5 6 7 1School of Basic Medical Sciences, Nanchang University, Nanchang, Jiangxi, 330031, China. 8 2Howard Hughes Medical Institute, Janelia Research Campus, Ashburn, VA 20147, USA 9 3Department of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, KY 10 40536, USA. 11 4Key Laboratory of Medical Electrophysiology, Ministry of Education, and Institute of 12 Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan, 646000, China 13 5The Key Laboratory of Molecular Medicine, the Second Affiliated Hospital of Nanchang 14 University, Nanchang 330006, China. 15 6Howard Hughes Medical Institute, Department of Biological Chemistry and Molecular 16 Pharmacology, Harvard Medical School, Boston, MA 02115, USA. 17 18 *These authors contributed equally to this work. 19 # Corresponding authors bioRxiv preprint doi: https://doi.org/10.1101/282715; this version posted March 15, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 20 Abstract 21 Members of the transient receptor potential (TRP) ion channels conduct cations into cells. They 22 mediate functions ranging from neuronally-mediated hot and cold sensation to intracellular 23 organellar and primary ciliary signaling. -
TRPM8 Channels and Dry Eye
UC Berkeley UC Berkeley Previously Published Works Title TRPM8 Channels and Dry Eye. Permalink https://escholarship.org/uc/item/2gz2d8s3 Journal Pharmaceuticals (Basel, Switzerland), 11(4) ISSN 1424-8247 Authors Yang, Jee Myung Wei, Edward T Kim, Seong Jin et al. Publication Date 2018-11-15 DOI 10.3390/ph11040125 Peer reviewed eScholarship.org Powered by the California Digital Library University of California pharmaceuticals Review TRPM8 Channels and Dry Eye Jee Myung Yang 1,2 , Edward T. Wei 3, Seong Jin Kim 4 and Kyung Chul Yoon 1,* 1 Department of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Korea; [email protected] 2 Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 34141, Korea 3 School of Public Health, University of California, Berkeley, CA 94720, USA; [email protected] 4 Department of Dermatology, Chonnam National University Medical School and Hospital, Gwangju 61469, Korea; [email protected] * Correspondence: [email protected] Received: 17 September 2018; Accepted: 12 November 2018; Published: 15 November 2018 Abstract: Transient receptor potential (TRP) channels transduce signals of chemical irritation and temperature change from the ocular surface to the brain. Dry eye disease (DED) is a multifactorial disorder wherein the eyes react to trivial stimuli with abnormal sensations, such as dryness, blurring, presence of foreign body, discomfort, irritation, and pain. There is increasing evidence of TRP channel dysfunction (i.e., TRPV1 and TRPM8) in DED pathophysiology. Here, we review some of this literature and discuss one strategy on how to manage DED using a TRPM8 agonist.