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Biomolecules
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Featured Papers in Ion Channels Diseases
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Featured Papers in Ion Channels Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: closed (10 October 2023) | Viewed by 13324

Special Issue Editors

Dr. Oleg Palygin

E-Mail Website
Guest Editor
Division of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC, USA
Interests: kidney; ion channels; ion transport; body electrolytes; mutations; oxidative stress; albuminuria
Dr. Mykola Mamenko

E-Mail Website
Guest Editor
Department of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA
Interests: collecting duct; hypertension; nephrogenic diabetes insipidus; calcium signaling; aldosterone

Special Issue Information

Dear Colleagues,

Ion channels span through the membrane to form pores, allowing selected ions to pass along their electrochemical gradient at a rate of up to 108 per second. Each ion channel is a multimeric assembly of pore-forming and, sometimes, accessory subunits encoded by more than 400 genes. The passage of ions through the pore is controlled by a "gate" that can be opened or closed by changes in membrane potential, ligand binding, intracellular second messengers and metabolites, phosphorylation, mechanical force, temperature, and other factors. Ion channels are present in all cell types and regulate almost every aspect of body function, including neurotransmission and muscle contraction, epithelial transport and immune cell activation, hormone secretion and cell volume, and tissue repair and development. The dysfunction or complete loss of ion channel subunits and proteins promotes positive or negative interaction with signal transduction, resulting in a range of diseases known as channelopathies. These disorders can be hereditary or acquired, and can manifest in hypertension, arrhythmias, skeletal dysplasia, paralysis, epilepsy, and cystic fibrosis, to name a few. This makes ion channels an attractive target for therapeutic intervention and future drug development.

We are pleased to invite you to submit your papers to this Special Issue entitled ‘Featured Reviews in Ion Channels Diseases’ which aims to collect high-quality review and research papers highlighting the latest developments in the field of ion channels and channelopathies. The topics of interest for this Special Issue include, but are not limited to:

  • Novel mutations in ion channels and pathophysiological function;
  • Ion transport and cell function in cell communication, homeostasis, and energy balance;
  • Ion channel pharmacology;
  • The origin and evolution of ion channels;
  • Ion channel modulation via intracellular signaling pathways (GPCR, β-arrestin, CaMKII, etc.);
  • Electrophysiology and calcium imaging for ion channel function.

We look forward to receiving your contributions.

Dr. Oleg Palygin
Dr. Mykola Mamenko
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 single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules 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

  • channelopathy
  • ion transport
  • electrophysiology
  • calcium imaging
  • pharmacology
  • genetics

Published Papers (6 papers)

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Research

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23 pages, 1601 KiB  
Article
Diabetes-Induced Amplification of Nociceptive DRG Neuron Output by Upregulation of Somatic T-Type Ca2+ Channels
by Arsentii Ivasiuk, Maksym Matvieienko, Nikolai I. Kononenko, Dmytro E. Duzhyy, Sergiy M. Korogod, Nana Voitenko and Pavel Belan
Biomolecules 2023, 13(9), 1320; https://doi.org/10.3390/biom13091320 - 28 Aug 2023
Cited by 1 | Viewed by 873
Abstract
The development of pain symptoms in peripheral diabetic neuropathy (PDN) is associated with the upregulation of T-type Ca2+ channels (T-channels) in the soma of nociceptive DRG neurons. Moreover, a block of these channels in DRG neurons effectively reversed mechanical and thermal hyperalgesia [...] Read more.
The development of pain symptoms in peripheral diabetic neuropathy (PDN) is associated with the upregulation of T-type Ca2+ channels (T-channels) in the soma of nociceptive DRG neurons. Moreover, a block of these channels in DRG neurons effectively reversed mechanical and thermal hyperalgesia in animal diabetic models, indicating that T-channel functioning in these neurons is causally linked to PDN. However, no particular mechanisms relating the upregulation of T-channels in the soma of nociceptive DRG neurons to the pathological pain processing in PDN have been suggested. Here we have electrophysiologically identified voltage-gated currents expressed in nociceptive DRG neurons and developed a computation model of the neurons, including peripheral and central axons. Simulations showed substantially stronger sensitivity of neuronal excitability to diabetes-induced T-channel upregulation at the normal body temperature compared to the ambient one. We also found that upregulation of somatic T-channels, observed in these neurons under diabetic conditions, amplifies a single action potential invading the soma from the periphery into a burst of multiple action potentials further propagated to the end of the central axon. We have concluded that the somatic T-channel-dependent amplification of the peripheral nociceptive input to the spinal cord demonstrated in this work may underlie abnormal nociception at different stages of diabetes development. Full article
(This article belongs to the Special Issue Featured Papers in Ion Channels Diseases)
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20 pages, 2427 KiB  
Article
Bidirectional TRP/L Type Ca2+ Channel/RyR/BKCa Molecular and Functional Signaloplex in Vascular Smooth Muscles
by Dariia O. Dryn, Mariia I. Melnyk, Donal Melanaphy, Igor V. Kizub, Christopher D. Johnson and Alexander V. Zholos
Biomolecules 2023, 13(5), 759; https://doi.org/10.3390/biom13050759 - 27 Apr 2023
Cited by 1 | Viewed by 1748
Abstract
TRP channels are expressed both in vascular myocytes and endothelial cells, but knowledge of their operational mechanisms in vascular tissue is particularly limited. Here, we show for the first time the biphasic contractile reaction with relaxation followed by a contraction in response to [...] Read more.
TRP channels are expressed both in vascular myocytes and endothelial cells, but knowledge of their operational mechanisms in vascular tissue is particularly limited. Here, we show for the first time the biphasic contractile reaction with relaxation followed by a contraction in response to TRPV4 agonist, GSK1016790A, in a rat pulmonary artery preconstricted with phenylephrine. Similar responses were observed both with and without endothelium, and these were abolished by the TRPV4 selective blocker, HC067047, confirming the specific role of TRPV4 in vascular myocytes. Using selective blockers of BKCa and L-type voltage-gated Ca2+ channels (CaL), we found that the relaxation phase was inducted by BKCa activation generating STOCs, while subsequent slowly developing TRPV4-mediated depolarisation activated CaL, producing the second contraction phase. These results are compared to TRPM8 activation using menthol in rat tail artery. Activation of both types of TRP channels produces highly similar changes in membrane potential, namely slow depolarisation with concurrent brief hyperpolarisations due to STOCs. We thus propose a general concept of bidirectional TRP-CaL-RyR-BKCa molecular and functional signaloplex in vascular smooth muscles. Accordingly, both TRPV4 and TRPM8 channels enhance local Ca2+ signals producing STOCs via TRP–RyR–BKCa coupling while simultaneously globally engaging BKCa and CaL channels by altering membrane potential. Full article
(This article belongs to the Special Issue Featured Papers in Ion Channels Diseases)
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14 pages, 1686 KiB  
Article
Long-Term Blockade of Nociceptive Nav1.7 Channels Is Analgesic in Rat Models of Knee Arthritis
by Allison R. Reid, Patrice D. Côté and Jason J. McDougall
Biomolecules 2022, 12(11), 1571; https://doi.org/10.3390/biom12111571 - 26 Oct 2022
Cited by 2 | Viewed by 1907
Abstract
The voltage gated sodium channels (Nav) 1.7, 1.8, and 1.9 are primarily located on nociceptors where they are involved in signalling neuropathic pain. This study examined the effect of Nav1.7 blockade on joint pain using either the small molecule [...] Read more.
The voltage gated sodium channels (Nav) 1.7, 1.8, and 1.9 are primarily located on nociceptors where they are involved in signalling neuropathic pain. This study examined the effect of Nav1.7 blockade on joint pain using either the small molecule inhibitor PF05089771 or an antibody directed towards the intracellular domain of the ion channel. Male Wistar rats were assigned to one of three experimental groups consisting of either intra-articular injection of 3 mg sodium monoiodoacetate (MIA—joint degeneration group), intra-articular injection of 100 μg lysophosphatidic acid (LPA—joint neuropathy group), or transection of the medial meniscus (MMT—posttraumatic osteoarthritis group). G-ratio calculations were performed to determine potential demyelination and immunohistochemistry was used to measure Nav1.7 expression on joint afferent cell bodies. Pain behaviour was evaluated over 3 h by von Frey hair algesiometry and hindlimb weight bearing before and after local administration of PF05089771 (0.1 mg/50 µL). Chronic pain behaviour was assessed over 28 days following peripheral treatment with a Nav1.7 antibody (Ab) in conjunction with the transmembrane carrier peptide Pep1. Demyelination and increased Nav1.7 channel expression were observed in MIA and LPA rats, but not with MMT. Acute secondary allodynia was diminished by PF05089771 while a single injection of Nav1.7 Ab-Pep1 reduced pain up to 28 days. This analgesia only occurred in MIA and LPA animals. Hindlimb incapacitance was not affected by any treatment. These data indicate that joint pain associated with neural demyelination can be alleviated somewhat by Nav1.7 channel blockade. Biologics that inactivate Nav1.7 channels have the potential to reduce arthritis pain over a protracted period of time. Full article
(This article belongs to the Special Issue Featured Papers in Ion Channels Diseases)
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Review

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14 pages, 1186 KiB  
Review
Modus operandi of ClC-K2 Cl− Channel in the Collecting Duct Intercalated Cells
by Anna Stavniichuk, Kyrylo Pyrshev, Viktor N. Tomilin, Mariya Kordysh, Oleg Zaika and Oleh Pochynyuk
Biomolecules 2023, 13(1), 177; https://doi.org/10.3390/biom13010177 - 14 Jan 2023
Cited by 1 | Viewed by 2477
Abstract
The renal collecting duct is known to play a critical role in many physiological processes, including systemic water–electrolyte homeostasis, acid–base balance, and the salt sensitivity of blood pressure. ClC-K2 (ClC-Kb in humans) is a Cl−-permeable channel expressed on the basolateral membrane [...] Read more.
The renal collecting duct is known to play a critical role in many physiological processes, including systemic water–electrolyte homeostasis, acid–base balance, and the salt sensitivity of blood pressure. ClC-K2 (ClC-Kb in humans) is a Cl−-permeable channel expressed on the basolateral membrane of several segments of the renal tubule, including the collecting duct intercalated cells. ClC-Kb mutations are causative for Bartters’ syndrome type 3 manifested as hypotension, urinary salt wasting, and metabolic alkalosis. However, little is known about the significance of the channel in the collecting duct with respect to the normal physiology and pathology of Bartters’ syndrome. In this review, we summarize the available experimental evidence about the signaling determinants of ClC-K2 function and the regulation by systemic and local factors as well as critically discuss the recent advances in understanding the collecting-duct-specific roles of ClC-K2 in adaptations to changes in dietary Cl− intake and maintaining systemic acid–base homeostasis. Full article
(This article belongs to the Special Issue Featured Papers in Ion Channels Diseases)
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18 pages, 2288 KiB  
Review
The Effects of TRPC6 Knockout in Animal Models of Kidney Disease
by Stuart E. Dryer and Eun Young Kim
Biomolecules 2022, 12(11), 1710; https://doi.org/10.3390/biom12111710 - 18 Nov 2022
Cited by 5 | Viewed by 2130
Abstract
Diseases that induce a loss of renal function affect a substantial portion of the world’s population and can range from a slight decline in the glomerular filtration rate or microalbuminuria to complete kidney failure. Kidney disorders can be acute or chronic, but any [...] Read more.
Diseases that induce a loss of renal function affect a substantial portion of the world’s population and can range from a slight decline in the glomerular filtration rate or microalbuminuria to complete kidney failure. Kidney disorders can be acute or chronic, but any significant reduction in renal function is associated with increased all-cause morbidity and mortality, especially when the conditions become chronic. There is an urgent need for new therapeutic approaches to slow or halt the progression of kidney disease. One potential target of considerable interest is the canonical transient receptor potential-6 (TRPC6) channel. TRCP6 is a cationic channel with a significant permeability to Ca2+. It is expressed in several tissues, including in multiple cell types of the kidney in glomeruli, microvasculature, and tubules. Here, we will describe TRPC6 channels and their roles in signal transduction, with an emphasis on renal cells, and the studies implicating TRPC6 channels in the progression of inherited and acquired kidney diseases. We then describe studies using TRPC6 knockout mice and rats subjected to treatments that model human diseases, including nephrotic syndromes, diabetic nephropathy, autoimmune glomerulonephritis, and acute kidney injuries induced by renal ischemia and by obstruction of the urinary tract. TRPC6 knockout has been shown to reduce glomerular manifestations of disease in several of these models and reduces renal fibrosis caused by urinary tract obstruction. TRPC6 knockout has proven to be less effective at reducing diabetic nephropathy in mouse and rat models. We also summarize the implications of these studies for drug development. Full article
(This article belongs to the Special Issue Featured Papers in Ion Channels Diseases)
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15 pages, 361 KiB  
Review
Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation
by Balázs Sonkodi
Biomolecules 2022, 12(9), 1207; https://doi.org/10.3390/biom12091207 - 31 Aug 2022
Cited by 15 | Viewed by 3599
Abstract
Piezo2 transmembrane excitatory mechanosensitive ion channels were identified as the principal mechanotransduction channels for proprioception. Recently, it was postulated that Piezo2 channels could be acutely microdamaged on an autologous basis at proprioceptive Type Ia terminals in a cognitive demand-induced acute stress response time [...] Read more.
Piezo2 transmembrane excitatory mechanosensitive ion channels were identified as the principal mechanotransduction channels for proprioception. Recently, it was postulated that Piezo2 channels could be acutely microdamaged on an autologous basis at proprioceptive Type Ia terminals in a cognitive demand-induced acute stress response time window when unaccustomed or strenuous eccentric contractions are executed. One consequence of this proposed transient Piezo2 microinjury could be a VGLUT1/Ia synaptic disconnection on motoneurons, as we can learn from platinum-analogue chemotherapy. A secondary, harsher injury phase with the involvement of polymodal Aδ and nociceptive C-fibers could follow the primary impairment of proprioception of delayed onset muscle soreness. Repetitive reinjury of these channels in the form of repeated bout effects is proposed to be the tertiary injury phase. Notably, the use of proprioception is associated with motor learning and memory. The impairment of the monosynaptic static phase firing sensory encoding of the affected stretch reflex could be the immediate consequence of the proposed Piezo2 microdamage leading to impaired proprioception, exaggerated contractions and reduced range of motion. These transient Piezo2 channelopathies in the primary afferent terminals could constitute the critical gateway to the pathophysiology of delayed onset muscle soreness. Correspondingly, fatiguing eccentric contraction-based pathological hyperexcitation of the Type Ia afferents induces reactive oxygen species production-associated neuroinflammation and neuronal activation in the spinal cord of delayed onset muscle soreness. Full article
(This article belongs to the Special Issue Featured Papers in Ion Channels Diseases)
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