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Advanced Science (Weinheim,... Aug 2022Ion transport under nanoconfined spaces is a ubiquitous phenomenon in nature and plays an important role in the energy conversion and signal transduction processes of... (Review)
Review
Ion transport under nanoconfined spaces is a ubiquitous phenomenon in nature and plays an important role in the energy conversion and signal transduction processes of both biological and artificial systems. Unlike the free diffusion in continuum media, anomalous behaviors of ions are often observed in nanostructured systems, which is governed by the complex interplay between various interfacial interactions. Conventionally, nanoionics mainly refers to the study of ion transport in solid-state nanosystems. In this review, to extent this concept is proposed and a new framework to understand the phenomena, mechanism, methodology, and application associated with ion transport at the nanoscale is put forward. Specifically, here nanoionics is summarized into three categories, i.e., biological, artificial, and hybrid, and discussed the characteristics of each system. Compared with nanoelectronics, nanoionics is an emerging research field with many theoretical and practical challenges. With this forward-looking perspective, it is hoped that nanoionics can attract increasing attention and find wide range of applications as nanoelectronics.
Topics: Diffusion; Ion Transport; Ions; Nanostructures
PubMed: 35723422
DOI: 10.1002/advs.202200534 -
Medicina 2019The chloride channels, sodium and bicarbonate channels, and aquaporin water channels are coordinated to maintain the airway surface liquid that is necessary for... (Review)
Review
The chloride channels, sodium and bicarbonate channels, and aquaporin water channels are coordinated to maintain the airway surface liquid that is necessary for mucociliary clearance. The general mechanism for the transport of electrolytes and fluids depends mainly on the differential expression and distribution of ion transporters and pumps. Ions and water move through the paracellular or transcellular pathways. The transcellular route of electrolyte transport requires an active transport (dependent on ATP) or passive (following electrochemical gradients) of ions. The paracellular pathway is a passive process that is ultimately controlled by the predominant transepithelial electrochemical gradients. Cystic fibrosis is a hereditary disease that is produced by mutations in the gene that encode cystic fibrosis transmembrane conductance regulatory protein (CFTR) that acts as a chloride channel and performs functions of hydration of periciliary fluid and maintenance of luminal pH. The dysfunction of the chlorine channel in the respiratory epithelium determines an alteration in the bronchial secretions, with an increase in its viscosity and alteration of the mucociliary clearance and that associated with infectious processes can lead to irreversible lung damage. CFTR dysfunction has also been implicated in the pathogenesis of acute pancreatitis, chronic obstructive pulmonary disease, and bronchial hyperreactivity in asthma. There are drugs that exploit physiological mechanisms in the transport of ions with a therapeutic objective.
Topics: Biological Transport, Active; Chloride Channels; Cystic Fibrosis; Cystic Fibrosis Transmembrane Conductance Regulator; Humans; Ion Transport; Mucociliary Clearance
PubMed: 31487254
DOI: No ID Found -
American Journal of Physiology. Lung... Nov 2017Maintenance of normal epithelial ion and water transport in the lungs includes providing a thin layer of surface liquid that coats the conducting airways. This airway... (Review)
Review
Maintenance of normal epithelial ion and water transport in the lungs includes providing a thin layer of surface liquid that coats the conducting airways. This airway surface liquid is critical for normal lung function in a number of ways but, perhaps most importantly, is required for normal mucociliary clearance and bacterial removal. Preservation of the appropriate level of hydration, pH, and viscosity for the airway surface liquid requires the proper regulation and function of a battery of different types of ion channels and transporters. Here we discuss how alterations in ion channel/transporter function often lead to lung pathologies.
Topics: Animals; Biological Transport; Humans; Ion Channels; Ion Transport; Lung; Mucociliary Clearance; Respiratory Mucosa
PubMed: 29025712
DOI: 10.1152/ajplung.00285.2017 -
The Journal of General Physiology Jun 2015Interaction of multiple ligands with a protein or protein complex is a widespread phenomenon that allows for cooperativity. Here, we review the use of the Hill equation,... (Review)
Review
Interaction of multiple ligands with a protein or protein complex is a widespread phenomenon that allows for cooperativity. Here, we review the use of the Hill equation, which is commonly used to analyze binding or kinetic data, to analyze the kinetics of ion-coupled transporters and show how the mechanism of transport affects the Hill coefficient. Importantly, the Hill analysis of ion-coupled transporters can provide the exact number of transported co-ions, regardless of the extent of the cooperativity in ion binding.
Topics: Animals; Binding Sites; Cell Membrane; Humans; Ion Channel Gating; Ion Transport; Kinetics; Ligands; Membrane Potentials; Models, Biological; Protein Binding; Symporters
PubMed: 26009547
DOI: 10.1085/jgp.201411332 -
Experimental Physiology Apr 2016What is the topic of this review? Sensing the amount of ingested sodium is one mechanism by which sodium balance is regulated. This review describes the role of gastrin... (Review)
Review
What is the topic of this review? Sensing the amount of ingested sodium is one mechanism by which sodium balance is regulated. This review describes the role of gastrin in the cross-talk between the stomach and the kidney following the ingestion of sodium. What advances does it highlight? Neural mechanisms and several gut hormones, including cholecystokinin and uroguanylin, have been suggested to mediate the natriuresis after an oral sodium load. It is proposed that gastrin produced by G-cells via its receptor, cholecystokinin B receptor, interacts with renal D1 -like dopamine receptors to increase renal sodium excretion. Hypertension develops with chronically increased sodium intake when sodium that accumulates in the body can no longer be sequestered, extracellular fluid volume is expanded, and compensatory neural, hormonal and pressure-natriuresis mechanisms fail. Sensing the amount of ingested sodium, by the stomach, is one mechanism by which sodium balance is regulated. The natriuresis following the ingestion of a certain amount of sodium may be due to an enterokine, gastrin, secreted by G-cells in the stomach and duodenum and released into the circulation. Circulating gastrin levels are 10- to 20-fold higher than those for cholecystokinin. Of all the gut hormones circulating in the plasma, gastrin is the one that is reabsorbed to the greatest extent by renal tubules. Gastrin, via its receptor, the cholecystokinin type B receptor (CCKBR), is natriuretic in mammals, including humans, by inhibition of renal sodium transport. Germline deletion of gastrin (Gast) or Cckbr gene in mice causes salt-sensitive hypertension. Selective silencing of Gast in the stomach and duodenum impairs the ability to excrete an oral sodium load and also increases blood pressure. Thus, the gastrorenal axis, mediated by gastrin, can complement pronatriuretic hormones, such as dopamine, to increase sodium excretion after an oral sodium load. These studies in mice may be translatable to humans because the chromosomal loci of CCKBR and GAST are linked to human essential hypertension. Understanding the role of genes in the regulation of renal function and blood pressure may lead to the tailoring of antihypertensive treatment based on genetic make-up.
Topics: Animals; Cholecystokinin; Gastrointestinal Tract; Homeostasis; Humans; Ion Transport; Kidney; Sodium
PubMed: 26854262
DOI: 10.1113/EP085286 -
WormBook : the Online Review of C.... Dec 2014The facilitated movement of ions across cell membranes can be characterized as occurring through active (ATP-dependent), secondary active (coupled), or passive transport... (Review)
Review
The facilitated movement of ions across cell membranes can be characterized as occurring through active (ATP-dependent), secondary active (coupled), or passive transport processes. Each of these processes is mediated by a diverse group of membrane proteins. Over the past fifteen years, studies of membrane transport in C. elegans have benefited from the fact that worms are anatomically simple, easily and economically cultured, and genetically tractable. These experimental advantages have been instrumental in defining how membrane transport processes contribute to whole organism physiology. The focus of this review is to survey the recent advances in our understanding of membrane transport that have arisen from integrative physiological approaches in the nematode C. elegans.
Topics: Animals; Caenorhabditis elegans; Calcium Signaling; Cell Membrane; Ion Transport
PubMed: 25536490
DOI: 10.1895/wormbook.1.174.1 -
The Journal of Physiology Sep 2015The reabsorptive activity of renal proximal tubule cells is mediated by receptor-mediated endocytosis and polarized transport systems that reflect final cell... (Review)
Review
KEY POINTS
The reabsorptive activity of renal proximal tubule cells is mediated by receptor-mediated endocytosis and polarized transport systems that reflect final cell differentiation. Loss-of-function mutations of the endosomal chloride-proton exchanger ClC-5 (Dent's disease) cause a major trafficking defect in proximal tubule cells, associated with lysosomal dysfunction, oxidative stress and dedifferentiation/proliferation. A similar but milder defect is associated with mutations in CFTR (cystic fibrosis transmembrane conductance regulator). Vesicular chloride transport appears to be important for the integrity of the endolysosomal pathway in epithelial cells.
ABSTRACT
The epithelial cells lining the proximal tubules of the kidney reabsorb a large amount of filtered ions and solutes owing to receptor-mediated endocytosis and polarized transport systems that reflect final cell differentiation. Dedifferentiation of proximal tubule cells and dysfunction of receptor-mediated endocytosis characterize Dent's disease, a rare disorder caused by inactivating mutations in the CLCN5 gene that encodes the endosomal chloride-proton exchanger, ClC-5. The disease is characterized by a massive urinary loss of solutes (renal Fanconi syndrome), with severe metabolic complications and progressive renal failure. Investigations of mutations affecting the gating of ClC-5 revealed that the proximal tubule dysfunction may occur despite normal endosomal acidification. In addition to defective endocytosis, proximal tubule cells lacking ClC-5 show a trafficking defect in apical receptors and transporters, as well as lysosomal dysfunction and typical features of dedifferentiation, proliferation and oxidative stress. A similar but milder defect is observed in mouse models with defective CFTR, a chloride channel that is also expressed in the endosomes of proximal tubule cells. These data suggest a major role for endosomal chloride transport in the maintenance of epithelial differentiation and reabsorption capacity of the renal proximal tubule.
Topics: Animals; Chloride Channels; Chlorides; Endocytosis; Endosomes; Epithelial Cells; Humans; Ion Transport; Kidney Tubules, Proximal
PubMed: 25820368
DOI: 10.1113/JP270087 -
International Journal of Molecular... Nov 2016The membrane-bound sodium-calcium exchanger (NCX) proteins shape Ca homeostasis in many cell types, thus participating in a wide range of physiological and pathological... (Review)
Review
The membrane-bound sodium-calcium exchanger (NCX) proteins shape Ca homeostasis in many cell types, thus participating in a wide range of physiological and pathological processes. Determination of the crystal structure of an archaeal NCX (NCX_Mj) paved the way for a thorough and systematic investigation of ion transport mechanisms in NCX proteins. Here, we review the data gathered from the X-ray crystallography, molecular dynamics simulations, hydrogen-deuterium exchange mass-spectrometry (HDX-MS), and ion-flux analyses of mutants. Strikingly, the apo NCX_Mj protein exhibits characteristic patterns in the local backbone dynamics at particular helix segments, thereby possessing characteristic HDX profiles, suggesting structure-dynamic preorganization (geometric arrangements of catalytic residues before the transition state) of conserved α₁ and α₂ repeats at ion-coordinating residues involved in transport activities. Moreover, dynamic preorganization of local structural entities in the apo protein predefines the status of ion-occlusion and transition states, even though Na⁺ or Ca binding modifies the preceding backbone dynamics nearby functionally important residues. Future challenges include resolving the structural-dynamic determinants governing the ion selectivity, functional asymmetry and ion-induced alternating access. Taking into account the structural similarities of NCX_Mj with the other proteins belonging to the Ca/cation exchanger superfamily, the recent findings can significantly improve our understanding of ion transport mechanisms in NCX and similar proteins.
Topics: Amino Acid Sequence; Archaea; Calcium; Crystallography, X-Ray; Deuterium Exchange Measurement; Gene Expression; Homeostasis; Humans; Ion Transport; Molecular Dynamics Simulation; Mutation; Protein Domains; Protein Isoforms; Protein Structure, Secondary; Sodium; Sodium-Calcium Exchanger; Structure-Activity Relationship
PubMed: 27879668
DOI: 10.3390/ijms17111949 -
Signal Transduction and Targeted Therapy Apr 2023
Topics: Ion Transport; Thermodynamics
PubMed: 37055402
DOI: 10.1038/s41392-023-01361-3 -
Seminars in Nephrology Nov 2017Apolipoprotein L1 (APOL1) protein is the human serum factor that protect human beings against Trypanosoma brucei brucei, the cause of trypanosomiasis. Subspecies of T b... (Review)
Review
Apolipoprotein L1 (APOL1) protein is the human serum factor that protect human beings against Trypanosoma brucei brucei, the cause of trypanosomiasis. Subspecies of T b brucei that cause human sleeping sickness-T b gambiense and T b rhodesiense evolved molecular mechanisms that enabled them to evade killing by APOL1. Sequence changes (termed G1 and G2) in the APOL1 gene that restored its ability to kill T b rhodesiense also increase the risk of developing glomerular diseases and accelerate progression to end-stage kidney disease. To lyse trypanosome parasites, APOL1 forms pores in the trypanosome endolysosomal and mitochondrial membranes, resulting in rapid membrane depolarization. However, the molecular mechanism underlying APOL1 nephropathy is unknown. Recent experimental evidence has shown that aberrant efflux of intracellular potassium is an early event in APOL1-induced death of human embryonic kidney cells. Here, we discuss the possibility that abnormal efflux of cellular potassium or other cations may be relevant to the pathogenesis of APOL1 nephropathy.
Topics: Animals; Apolipoprotein L1; Cell Death; HEK293 Cells; Humans; Ion Channels; Ion Transport; Kidney Diseases; Mutation; Podocytes; Potassium
PubMed: 29110762
DOI: 10.1016/j.semnephrol.2017.07.008