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https://www.readbyqxmd.com/read/29326130/inward-rectifier-potassium-channels-kir2-x-and-caveolin-3-domain-specific-interaction-implications-for-purkinje-cell-dependent-ventricular-arrhythmias
#1
Ravi Vaidyanathan, Hanora Van Ert, Kazi T Haq, Stefano Morotti, Samuel Esch, Elise C McCune, Eleonora Grandi, Lee L Eckhardt
BACKGROUND: In human cardiac ventricle, IK1 is mainly comprised Kir2.1, but Kir2.2 and Kir2.3 heterotetramers occur and modulate IK1. Long-QT syndrome-9-associated CAV3 mutations cause decreased Kir2.1 current density, but Kir2.x heterotetramers have not been studied. Here, we determine the effect of long-QT syndrome-9-CAV3 mutation F97C on Kir2.x homo- and heterotetramers and model-associated arrhythmia mechanisms. METHODS AND RESULTS: Super-resolution microscopy, co-immunoprecipitation, cellular electrophysiology, on-cell Western blotting, and simulation of Purkinje and ventricular myocyte mathematical models were used...
January 2018: Circulation. Arrhythmia and Electrophysiology
https://www.readbyqxmd.com/read/29317494/hydrogen-sulfide-inhibits-kir2-and-kir3-channels-by-decreasing-sensitivity-to-the-phospholipid-pip2
#2
Junghoon Ha, Yu Xu, Takeharu Kawano, Tyler Hendon, Lia Baki, Sumanta Garai, Andreas Papapetropoulos, Ganesh Thakur, Leigh D Plant, Diomedes E Logothetis
Inwardly rectifying potassium (Kir) channels establish and regulate the resting membrane potential of excitable cells in the heart, brain and other peripheral tissues. Phosphatidylinositol 4,5-bisphosphate (PIP2) is a key direct activator of ion channels, including Kir channels. The gasotransmitter carbon monoxide has been shown to regulate Kir channel activity by altering channel-PIP2 interactions.  Here, we tested in two cellular models the effects and mechanism of action of another gasotransmitter, hydrogen sulfide (H2S), thought to play a key role in cellular responses under ischemic conditions...
January 9, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29290967/modelling-the-effects-of-chloroquine-on-kcnj2-linked-short-qt-syndrome
#3
Cunjin Luo, Kuanquan Wang, Henggui Zhang
A gain-of-function KCNJ2 D172N mutation in KCNJ2-encoded Kir2.1 channels underlies one form of short QT syndrome (SQT3), which is associated with increased susceptibility to arrhythmias and sudden death. Anti-malarial drug chloroquine was reported as an effective inhibitor of Kir2.1 channels. Using biophysically-detailed human ventricle computer models, this study assessed the effects of chloroquine on SQT3. The ten Tusscher et al. model of human ventricular cell action potential was modified to recapitulate functional changes in the inward rectifier K+ current (IK1) due to heterozygous and homozygous forms of the D172N mutation...
December 5, 2017: Oncotarget
https://www.readbyqxmd.com/read/29282531/kir2-1-channels-set-two-levels-of-resting-membrane-potential-with-inward-rectification
#4
Kuihao Chen, Dongchuan Zuo, Zheng Liu, Haijun Chen
Strong inward rectifier K+ channels (Kir2.1) mediate background K+ currents primarily responsible for maintenance of resting membrane potential. Multiple types of cells exhibit two levels of resting membrane potential. Kir2.1 and K2P1 currents counterbalance, partially accounting for the phenomenon of human cardiomyocytes in subphysiological extracellular K+ concentrations or pathological hypokalemic conditions. The mechanism of how Kir2.1 channels contribute to the two levels of resting membrane potential in different types of cells is not well understood...
December 27, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/29219824/thyrotoxic-periodic-paralysis-an-unusual-presentation-of-hyperthyroidism
#5
M Salih, C M J van Kinschot, R P Peeters, W W de Herder, E J J Duschek, J van der Linden, C van Noord
Thyrotoxic periodic paralysis (TPP) is a complication of hyperthyroidism among Asians, characterised by sudden onset of hypokalaemia and muscle paralysis. Several factors may contribute to a delay in diagnosis, including the subtlety of hyperthyroidism, the transient nature of the events and the rarity of this disease in the West. As life-threatening arrhythmias may occur during an attack, awareness among physicians is necessary for early recognition and treatment. Advances have been made in understanding the pathophysiological mechanism leading to hypokalaemia, which include recently identified mutations of the inwardly rectifying potassium channel Kir2...
October 2017: Netherlands Journal of Medicine
https://www.readbyqxmd.com/read/29212255/soluble-epoxide-hydrolase-inhibitors-t-aucb-regulated-microrna-1-and-its-target-genes-in-myocardial-infarction-mice
#6
Ya-Jun Gui, Tao Yang, Qiong Liu, Cai-Xiu Liao, Jing-Yuan Chen, Ya-Ting Wang, Jia-Hui Hu, Dan-Yan Xu
Purpose: Soluble epoxide hydrolase inhibitors (sEHIs) had been demonstrated to produce cardioprotective effects against ischemia-induced lethal arrhythmias, but the exact mechanisms remain unknown. The present study was designed to investigate whether the beneficial effects of sEHIs are related to regulation of microRNA-1, which was a proarrhythmic factor in the ischemic heart. Methods: A mousemyocardial infarction (MI) model was established by ligating the coronary artery...
November 7, 2017: Oncotarget
https://www.readbyqxmd.com/read/29205356/molecular-and-functional-characterization-of-inwardly-rectifying-k-currents-in-murine-proximal-colon
#7
Xu Huang, Si Hyung Lee, Hongli Lu, Kenton M Sanders, Sang Don Koh
Membrane potentials of gastrointestinal (GI) muscles are important because voltage dependent Ca2+ channels in smooth muscle cells (SMC) provide the Ca2+ that triggers contraction. Regulation of membrane potential is complicated because SMC are electrically coupled to interstitial cells of Cajal (ICC) and PDGFRα+ cells. Activation of conductances in any of these cells affects the excitability of the syncytium. We explored the role of inward rectifier K+ conductances in colonic ICC that might contribute to regulation of membrane potential...
December 3, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/29191750/sucrose-withdrawal-induces-depression-and-anxiety-like-behavior-by-kir2-1-upregulation-in-the-nucleus-accumbens
#8
Seonil Kim, Jiayi Shou, Sinedu Abera, Edward B Ziff
Dieting induces depression and anxiety among other emotional symptoms. Animal models indicate that repeated access to palatable foods such as sugar induces depression and anxiety-like behavior when the food is no longer available. However, the neurobiological mechanisms of how dietary restriction influences mood have not been fully understood. We used the two-bottle sucrose choice paradigm as an overeating and withdrawal model. Withdrawal after lengthy sucrose overeating elicited depression and anxiety-like behavior, which was reversed by sucrose reinstatement...
November 27, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/29184507/kir2-1-nav1-5-channel-complexes-are-differently-regulated-than-kir2-1-and-nav1-5-channels-alone
#9
Raquel G Utrilla, Paloma Nieto-Marín, Silvia Alfayate, David Tinaquero, Marcos Matamoros, Marta Pérez-Hernández, Sandra Sacristán, Lorena Ondo, Raquel de Andrés, F Javier Díez-Guerra, Juan Tamargo, Eva Delpón, Ricardo Caballero
Cardiac Kir2.1 and Nav1.5 channels generate the inward rectifier K+ (IK1) and the Na+ (INa) currents, respectively. There is a mutual interplay between the ventricular INa and IK1 densities, because Nav1.5 and Kir2.1 channels exhibit positive reciprocal modulation. Here we compared some of the biological properties of Nav1.5 and Kir2.1 channels when they are expressed together or separately to get further insights regarding their putative interaction. First we demonstrated by proximity ligation assays (PLAs) that in the membrane of ventricular myocytes Nav1...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/29055952/aloe-emodin-relieves-high-fat-diet-induced-qt-prolongation-via-mir-1-inhibition-and-ik1-up-regulation-in-rats
#10
Yan Bai, Zhenli Su, Hanqi Sun, Wei Zhao, Xue Chen, Pengzhou Hang, Wenliang Zhu, Zhimin Du
BACKGROUND/AIMS: High-fat diet (HFD) causes cardiac electrical remodeling and increases the risk of ventricular arrhythmias. Aloe-emodin (AE) is an anthraquinone component isolated from rhubarb and has a similar chemical structure with emodin. The protective effect of emodin against cardiac diseases has been reported in the literature. However, the cardioprotective property of AE is still unknown. The present study investigated the effect of AE on HFD-induced QT prolongation in rats. METHODS: Adult male Wistar rats were randomly divided into three groups: control, HFD, and AE-treatment groups...
October 20, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29021306/characterization-of-a-human-induced-pluripotent-stem-cell-derived-cardiomyocyte-model-for-the-study-of-variant-pathogenicity-validation-of-a-kcnj2-mutation
#11
Roselle Gélinas, Nabil El Khoury, Marie-A Chaix, Claudine Beauchamp, Azadeh Alikashani, Nathalie Ethier, Gabrielle Boucher, Louis Villeneuve, Laura Robb, Frédéric Latour, Blandine Mondesert, Lena Rivard, Philippe Goyette, Mario Talajic, Céline Fiset, John David Rioux
BACKGROUND: Long-QT syndrome is a potentially fatal condition for which 30% of patients are without a genetically confirmed diagnosis. Rapid identification of causal mutations is thus a priority to avoid at-risk situations that can lead to fatal cardiac events. Massively parallel sequencing technologies are useful for the identification of sequence variants; however, electrophysiological testing of newly identified variants is crucial to demonstrate causality. Long-QT syndrome could, therefore, benefit from having a standardized platform for functional characterization of candidate variants in the physiological context of human cardiomyocytes...
October 2017: Circulation. Cardiovascular Genetics
https://www.readbyqxmd.com/read/29020060/phosphatidylinositol-4-5-bisphosphate-is-required-for-kcnq1-kcne1-channel-function-but-not-anterograde-trafficking
#12
Alice A Royal, Andrew Tinker, Stephen C Harmer
The slow delayed-rectifier potassium current (IKs) is crucial for human cardiac action potential repolarization. The formation of IKs requires co-assembly of the KCNQ1 α-subunit and KCNE1 β-subunit, and mutations in either of these subunits can lead to hereditary long QT syndrome types 1 and 5, respectively. It is widely recognised that the KCNQ1/KCNE1 (Q1/E1) channel requires phosphatidylinositol-4,5-bisphosphate (PIP2) binding for function. We previously identified a cluster of basic residues in the proximal C-terminus of KCNQ1 that form a PIP2/phosphoinositide binding site...
2017: PloS One
https://www.readbyqxmd.com/read/29018970/andersen-s-syndrome-mutants-produce-a-knockdown-of-inwardly-rectifying-k-channel-in-mouse-skeletal-muscle-in-vivo
#13
Dina Simkin, Gaëlle Robin, Serena Giuliano, Ana Vukolic, Pamela Moceri, Nicolas Guy, Kay-Dietrich Wagner, Alain Lacampagne, Bruno Allard, Saïd Bendahhou
Andersen's syndrome (AS) is a rare autosomal disorder that has been defined by the triad of periodic paralysis, cardiac arrhythmia, and developmental anomalies. AS has been directly linked to over 40 different autosomal dominant negative loss-of-function mutations in the KCNJ2 gene, encoding for the tetrameric strong inward rectifying K(+) channel KIR2.1. While KIR2.1 channels have been suggested to contribute to setting the resting membrane potential (RMP) and to control the duration of the action potential (AP) in skeletal and cardiac muscle, the mechanism by which AS mutations produce such complex pathophysiological symptoms is poorly understood...
October 10, 2017: Cell and Tissue Research
https://www.readbyqxmd.com/read/29017447/characterization-of-a-novel-kcnj2-sequence-variant-detected-in-andersen-tawil-syndrome-patients
#14
Stefanie Scheiper, Brigitte Hertel, Britt-Maria Beckmann, Stefan Kääb, Gerhard Thiel, Silke Kauferstein
BACKGROUND: Mutations in the KCNJ2 gene encoding the ion channel Kir2.1 have been linked to the Andersen-Tawil syndrome (ATS). Molecular genetic screening performed in a family exhibiting clinical ATS phenotypes unmasked a novel sequence variant (c.434A > G, p.Y145C) in this gene. The aim of this study was to investigate the effect of this variant on Kir2.1 ion channel functionality. METHODS: Mutant as well as wild type GFP tagged Kir2.1 channels were expressed in HEK293 cells...
October 10, 2017: BMC Medical Genetics
https://www.readbyqxmd.com/read/28957802/overexpression-of-m3-muscarinic-receptor-suppressed-adverse-electrical-remodeling-in-hypertrophic-myocardium-via-increasing-repolarizing-k-currents
#15
Xue Chen, Yan Bai, Hanqi Sun, Zhenli Su, Jing Guo, Chuan Sun, Zhimin Du
BACKGROUND/AIMS: Cardiac hypertrophy (CH) is an adaptive response to diverse cardiovascular conditions, which is accompanied by adverse electrical remodeling manifested as abnormal K+ channel activities. M3 subtype of muscarinic acetylcholine receptor (M3-mAChR) is a novel regulator of cardiac electrical activity. In this study we aim to explore if the overexpression of M3-mAChR could attenuate the adverse electrical remodeling in CH and then uncover its underlying electrophysiological mechanisms...
2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28863819/differential-effects-of-sterols-on-ion-channels-stereospecific-binding-vs-stereospecific-response
#16
Nicolas Barbera, Manuela A A Ayee, Belinda S Akpa, Irena Levitan
Numerous ion channels have been shown to be regulated by the level of membrane cholesterol, but the mechanisms responsible for these effects are still not well understood. The key question in the field is how to discriminate between the contributions of the two central mechanisms that might be responsible for the sensitivity of ion channels to cholesterol: specific sterol-protein interactions or regulation of channels by the bilayer physical properties. Comparative analysis of cholesterol and its isomers on the function of an ion channel is a powerful tool to achieve this goal...
2017: Current Topics in Membranes
https://www.readbyqxmd.com/read/28863816/insights-into-the-molecular-requirements-for-cholesterol-binding-to-ion-channels
#17
Avia Rosenhouse-Dantsker
The concept that cholesterol binds to proteins via specific binding motifs, and thereby modulates their function, has emerged two decades ago. When we recently embarked on studies to uncover the putative binding region(s) of cholesterol in the Kir2.1 channel, we carried out an unbiased approach that combines computational and experimental methods. This approach resulted in the identification of novel cholesterol-binding regions distinct from known cholesterol-binding motifs. In recent years, a plethora of structures of proteins complexed with cholesterol have been determined revealing variegated cholesterol-binding regions that can provide invaluable insights into the prerequisites for cholesterol binding...
2017: Current Topics in Membranes
https://www.readbyqxmd.com/read/28830445/responses-of-rat-and-mouse-primary-microglia-to-pro-and-anti-inflammatory-stimuli-molecular-profiles-k-channels-and-migration
#18
Doris Lam, Starlee Lively, Lyanne C Schlichter
BACKGROUND: Acute CNS damage is commonly studied using rat and mouse models, but increasingly, molecular analysis is finding species differences that might affect the ability to translate findings to humans. Microglia can undergo complex molecular and functional changes, often studied by in vitro responses to discrete activating stimuli. There is considerable evidence that pro-inflammatory (M1) activation can exacerbate tissue damage, while anti-inflammatory (M2) states help resolve inflammation and promote tissue repair...
August 22, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28812984/modelling-the-effects-of-quinidine-disopyramide-and-e-4031-on-short-qt-syndrome-variant-3-in-the-human-ventricles
#19
Cunjin Luo, Kuanquan Wang, Henggui Zhang
Short QT syndrome (SQTS) is an inherited cardiac channelopathy, but at present little information is available on its pharmacological treatment. SQT3 variant (linked to the inward rectifier potassium current IK1) of SQTS, results from a gain-of-function mutation (Kir2.1 D172N) in the KCNJ2-encoded channels, which is associated with ventricular fibrillation (VF). Using biophysically-detailed human ventricular computer models, this study investigated the potential effects of quinidine, disopyramide, and E-4031 on SQT3...
August 16, 2017: Physiological Measurement
https://www.readbyqxmd.com/read/28749940/upregulation-of-an-inward-rectifying-k-channel-can-rescue-slow-ca2-oscillations-in-k-atp-channel-deficient-pancreatic-islets
#20
Vehpi Yildirim, Suryakiran Vadrevu, Benjamin Thompson, Leslie S Satin, Richard Bertram
Plasma insulin oscillations are known to have physiological importance in the regulation of blood glucose. In insulin-secreting β-cells of pancreatic islets, K(ATP) channels play a key role in regulating glucose-dependent insulin secretion. In addition, they convey oscillations in cellular metabolism to the membrane by sensing adenine nucleotides, and are thus instrumental in mediating pulsatile insulin secretion. Blocking K(ATP) channels pharmacologically depolarizes the β-cell plasma membrane and terminates islet oscillations...
July 2017: PLoS Computational Biology
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