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Ion Transporters and Channels in Physiology and Pathophysiology 2.0: from Molecules to Whole Bodies

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (28 June 2019) | Viewed by 23195

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Special Issue Editor

Prof. Dr. Yoshinori Marunaka

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Guest Editor

1. Medical Research Institute, Kyoto Industrial Health Association, Kyoto 604-8472, Japan
2. Research Organization of Science and Technology, Ritsumeikan University, Kusatsu 525-8577, Japan
3. Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 802-8566, Japan
Interests: diabetes mellitus; cancer; ion environments; pH regulation; food factor
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Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our 2017 Special Issue, "Ion Transporters and Channels in Physiology and Pathophysiology" (https://www.mdpi.com/journal/ijms/special_issues/itc).

Ion transport across cell membranes, mediated by ion transporters and channels, play important roles in the control of bodily and cellular functions, such as the actions of hormones and enzymes, cell growth, including aberrant cancer cell proliferation, neurite elongation, and transepithelial ion and water transport, which is crucial for blood pressure control, electrolyte homeostasis, airway immunity, and so on. Recent advances in this research field have led us to the recognition of ion transporters and channels as pharmacological targets for treatment of various diseases, including hypertension, cancer, diabetes mellitus, lung edema, infection, etc.

We invite authors to submit original research and review articles providing or summarizing new knowledge on various aspects of ion transporters and channels. Although studies on their physiological and pathophysiological roles are encouraged, pharmacological, biochemical, and biophysical studies are also welcome to be published in this Special Issue. Papers related to any aspect of ion transporters and channels will be considered for this Special Issue.

Prof. Dr. Yoshinori Marunaka
Guest Editor

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

epithelial ion transport
ion transporters
ion channels

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Published Papers (5 papers)

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Research

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19 pages, 3230 KiB

Open AccessArticle

Acid- and Volume-Sensitive Chloride Currents in Microglial Cells

by Michael Kittl, Katharina Helm, Marlena Beyreis, Christian Mayr, Martin Gaisberger, Martina Winklmayr, Markus Ritter and Martin Jakab

Int. J. Mol. Sci. 2019, 20(14), 3475; https://doi.org/10.3390/ijms20143475 - 15 Jul 2019

Cited by 12 | Viewed by 3152

Abstract

Many cell types express an acid-sensitive outwardly rectifying (ASOR) anion current of an unknown function. We characterized such a current in BV-2 microglial cells and then studied its interrelation with the volume-sensitive outwardly rectifying (VSOR) Cl⁻ current and the effect of acidosis on cell volume regulation. We used patch clamp, the Coulter method, and the pH-sensitive dye BCECF to measure Cl⁻ currents and cell membrane potentials, mean cell volume, and intracellular pH, respectively. The ASOR current activated at pH ≤ 5.0 and displayed an I⁻ > Cl⁻ > gluconate⁻ permeability sequence. When compared to the VSOR current, it was similarly sensitive to DIDS, but less sensitive to DCPIB, and insensitive to tamoxifen. Under acidic conditions, the ASOR current was the dominating Cl⁻ conductance, while the VSOR current was apparently inactivated. Acidification caused cell swelling under isotonic conditions and prevented the regulatory volume decrease under hypotonicity. We conclude that acidification, associated with activation of the ASOR- and inactivation of the VSOR current, massively impairs cell volume homeostasis. ASOR current activation could affect microglial function under acidotoxic conditions, since acidosis is a hallmark of pathophysiological events like inflammation, stroke or ischemia and migration and phagocytosis in microglial cells are closely related to cell volume regulation. Full article

(This article belongs to the Special Issue Ion Transporters and Channels in Physiology and Pathophysiology 2.0: from Molecules to Whole Bodies)

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24 pages, 3157 KiB

Open AccessArticle

Mechanisms Underlying Spontaneous Action Potential Generation Induced by Catecholamine in Pulmonary Vein Cardiomyocytes: A Simulation Study

by Shohei Umehara, Xiaoqiu Tan, Yosuke Okamoto, Kyoichi Ono, Akinori Noma, Akira Amano and Yukiko Himeno

Int. J. Mol. Sci. 2019, 20(12), 2913; https://doi.org/10.3390/ijms20122913 - 14 Jun 2019

Cited by 5 | Viewed by 3925

Abstract

Cardiomyocytes and myocardial sleeves dissociated from pulmonary veins (PVs) potentially generate ectopic automaticity in response to noradrenaline (NA), and thereby trigger atrial fibrillation. We developed a mathematical model of rat PV cardiomyocytes (PVC) based on experimental data that incorporates the microscopic framework of the local control theory of Ca²⁺ release from the sarcoplasmic reticulum (SR), which can generate rhythmic Ca²⁺ release (limit cycle revealed by the bifurcation analysis) when total Ca²⁺ within the cell increased. Ca²⁺ overload in SR increased resting Ca²⁺ efflux through the type II inositol 1,4,5-trisphosphate (IP₃) receptors (InsP₃R) as well as ryanodine receptors (RyRs), which finally triggered massive Ca²⁺ release through activation of RyRs via local Ca²⁺ accumulation in the vicinity of RyRs. The new PVC model exhibited a resting potential of −68 mV. Under NA effects, repetitive Ca²⁺ release from SR triggered spontaneous action potentials (APs) by evoking transient depolarizations (TDs) through Na⁺/Ca²⁺ exchanger (AP_TDs). Marked and variable latencies initiating AP_TDs could be explained by the time courses of the α1- and β1-adrenergic influence on the regulation of intracellular Ca²⁺ content and random occurrences of spontaneous TD activating the first AP_TD. Positive and negative feedback relations were clarified under AP_TD generation. Full article

(This article belongs to the Special Issue Ion Transporters and Channels in Physiology and Pathophysiology 2.0: from Molecules to Whole Bodies)

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19 pages, 3949 KiB

Open AccessArticle

FKBP8 Enhances Protein Stability of the CLC-1 Chloride Channel at the Plasma Membrane

by Yi-Jheng Peng, Yi-Ching Lee, Ssu-Ju Fu, Yun-Chia Chien, Yi-Fan Liao, Tsung-Yu Chen, Chung-Jiuan Jeng and Chih-Yung Tang

Int. J. Mol. Sci. 2018, 19(12), 3783; https://doi.org/10.3390/ijms19123783 - 28 Nov 2018

Cited by 7 | Viewed by 4757

Abstract

Mutations in the skeletal muscle-specific CLC-1 chloride channel are associated with the human hereditary disease myotonia congenita. The molecular pathophysiology underlying some of the disease-causing mutations can be ascribed to defective human CLC-1 protein biosynthesis. CLC-1 protein folding is assisted by several molecular chaperones and co-chaperones, including FK506-binding protein 8 (FKBP8). FKBP8 is generally considered an endoplasmic reticulum- and mitochondrion-resident membrane protein, but is not thought to contribute to protein quality control at the cell surface. Herein, we aim to test the hypothesis that FKBP8 may regulate CLC-1 protein at the plasma membrane. Surface biotinylation and subcellular fractionation analyses reveal that a portion of FKBP8 is present at the plasma membrane, and that co-expression with CLC-1 enhances surface localization of FKBP8. Immunoblotting analyses of plasma membrane proteins purified from skeletal muscle further confirm surface localization of FKBP8. Importantly, FKBP8 promotes CLC-1 protein stability at the plasma membrane. Together, our data underscore the importance of FKBP8 in the peripheral quality control of CLC-1 channel. Full article

(This article belongs to the Special Issue Ion Transporters and Channels in Physiology and Pathophysiology 2.0: from Molecules to Whole Bodies)

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18 pages, 6867 KiB

Open AccessArticle

Daidzein-Stimulated Increase in the Ciliary Beating Amplitude via an [Cl⁻]_i Decrease in Ciliated Human Nasal Epithelial Cells

by Taka-aki Inui, Makoto Yasuda, Shigeru Hirano, Yukiko Ikeuchi, Haruka Kogiso, Toshio Inui, Yoshinori Marunaka and Takashi Nakahari

Int. J. Mol. Sci. 2018, 19(12), 3754; https://doi.org/10.3390/ijms19123754 - 26 Nov 2018

Cited by 8 | Viewed by 3320

Abstract

The effects of the isoflavone daidzein on the ciliary beat distance (CBD, which is a parameter assessing the amplitude of ciliary beating) and the ciliary beat frequency (CBF) were examined in ciliated human nasal epithelial cells (cHNECs) in primary culture. Daidzein decreased [Cl⁻]_i and enhanced CBD in cHNECs. The CBD increase that was stimulated by daidzein was mimicked by Cl⁻-free NO₃⁻ solution and bumetanide (an inhibitor of Na⁺/K⁺/2Cl⁻ cotransport), both of which decreased [Cl⁻]_i. Moreover, the CBD increase was inhibited by 5-Nitro-2-(3-phenylpropylamino)benzoic acid (NPPB, a Cl⁻ channel blocker), which increased [Cl⁻]_i. CBF was also decreased by NPPB. The rate of [Cl⁻]_i decrease evoked by Cl⁻-free NO₃⁻ solution was enhanced by daidzein. These results suggest that daidzein activates Cl⁻ channels in cHNECs. Moreover, daidzein enhanced the microbead transport driven by beating cilia in the cell sheet of cHNECs, suggesting that an increase in CBD enhances ciliary transport. An [Cl⁻]_i decrease enhanced CBD, but not CBF, in cHNECs at 37 °C, although it enhanced both at 25 °C. Intracellular Cl⁻ affects both CBD and CBF in a temperature-dependent manner. In conclusion, daidzein, which activates Cl⁻ channels to decrease [Cl⁻]_i, stimulated CBD increase in cHNECs at 37 °C. CBD is a crucial factor that can increase ciliary transport in the airways under physiological conditions. Full article

(This article belongs to the Special Issue Ion Transporters and Channels in Physiology and Pathophysiology 2.0: from Molecules to Whole Bodies)

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Review

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22 pages, 4613 KiB

Open AccessReview

Ion Transporters, Channelopathies, and Glucose Disorders

by Huseyin Demirbilek, Sonya Galcheva, Dogus Vuralli, Sara Al-Khawaga and Khalid Hussain

Int. J. Mol. Sci. 2019, 20(10), 2590; https://doi.org/10.3390/ijms20102590 - 27 May 2019

Cited by 21 | Viewed by 7339

Abstract

Ion channels and transporters play essential roles in excitable cells including cardiac, skeletal and smooth muscle cells, neurons, and endocrine cells. In pancreatic beta-cells, for example, potassium K_ATP channels link the metabolic signals generated inside the cell to changes in the beta-cell membrane potential, and ultimately regulate insulin secretion. Mutations in the genes encoding some ion transporter and channel proteins lead to disorders of glucose homeostasis (hyperinsulinaemic hypoglycaemia and different forms of diabetes mellitus). Pancreatic K_ATP, Non-K_ATP, and some calcium channelopathies and MCT1 transporter defects can lead to various forms of hyperinsulinaemic hypoglycaemia (HH). Mutations in the genes encoding the pancreatic K_ATP channels can also lead to different types of diabetes (including neonatal diabetes mellitus (NDM) and Maturity Onset Diabetes of the Young, MODY), and defects in the solute carrier family 2 member 2 (SLC2A2) leads to diabetes mellitus as part of the Fanconi–Bickel syndrome. Variants or polymorphisms in some ion channel genes and transporters have been reported in association with type 2 diabetes mellitus. Full article

(This article belongs to the Special Issue Ion Transporters and Channels in Physiology and Pathophysiology 2.0: from Molecules to Whole Bodies)

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