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https://www.readbyqxmd.com/read/28636017/effect-of-cisplatin-on-the-transport-activity-of-pii-type-atpases
#1
Francesco Tadini-Buoninsegni, Giacomo Sordi, Serena Smeazzetto, Giovanni Natile, Fabio Arnesano
Cisplatin (cis-diamminedichlorido-Pt(ii)) is extensively used as a chemotherapeutic agent against various types of tumors. However, cisplatin administration causes serious side effects, including nephrotoxicity, ototoxicity and neurotoxicity. It has been shown that cisplatin can interact with P-type ATPases, e.g., Cu(+)-ATPases (ATP7A and ATP7B) and Na(+),K(+)-ATPase. Cisplatin-induced inhibition of Na(+),K(+)-ATPase has been related to the nephrotoxic effect of the drug. To investigate the inhibitory effects of cisplatin on the pumping activity of PII-type ATPases, electrical measurements were performed on sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) and Na(+),K(+)-ATPase embedded in vesicles/membrane fragments adsorbed on a solid-supported membrane...
June 21, 2017: Metallomics: Integrated Biometal Science
https://www.readbyqxmd.com/read/28630914/deregulated-ca-2-cycling-underlies-the-development-of-arrhythmia-and-heart-disease-due-to-mutant-obscurin
#2
Li-Yen R Hu, Maegen A Ackermann, Peter A Hecker, Benjamin L Prosser, Brendan King, Kelly A O'Connell, Alyssa Grogan, Logan C Meyer, Christopher E Berndsen, Nathan T Wright, W Jonathan Lederer, Aikaterini Kontrogianni-Konstantopoulos
Obscurins are cytoskeletal proteins with structural and regulatory roles encoded by OBSCN. Mutations in OBSCN are associated with the development of hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM). Specifically, the R4344Q mutation present in immunoglobulin domain 58 (Ig58) was the first to be linked with the development of HCM. To assess the effects of R4344Q in vivo, we generated the respective knock-in mouse model. Mutant obscurins are expressed and incorporated normally into sarcomeres...
June 2017: Science Advances
https://www.readbyqxmd.com/read/28630169/patient-specific-drug-screening-using-a-human-induced-pluripotent-stem-cell-model-of-catecholaminergic-polymorphic-ventricular-tachycardia-type-2
#3
Leonid Maizels, Irit Huber, Gil Arbel, Anke J Tijsen, Amira Gepstein, Asaad Khoury, Lior Gepstein
BACKGROUND: Catecholaminergic polymorphic ventricular tachycardia type 2 (CPVT2) results from autosomal recessive CASQ2 mutations, causing abnormal Ca(2+)-handling and malignant ventricular arrhythmias. We aimed to establish a patient-specific human induced pluripotent stem cell (hiPSC) model of CPVT2 and to use the generated hiPSC-derived cardiomyocytes to gain insights into patient-specific disease mechanism and pharmacotherapy. METHODS AND RESULTS: hiPSC cardiomyocytes were derived from a CPVT2 patient (D307H-CASQ2 mutation) and from healthy controls...
June 2017: Circulation. Arrhythmia and Electrophysiology
https://www.readbyqxmd.com/read/28630041/dysregulated-zn-2-homeostasis-impairs-cardiac-type-2-ryanodine-receptor-and-mitsugumin-23-functions-leading-to-sarcoplasmic-reticulum-ca-2-leakage
#4
Benedict Reilly-O'Donnell, Gavin B Robertson, Angela Karumbi, Connor McIntyre, Wojciech Bal, Miyuki Nishi, Hiroshi Takeshima, Alan J Stewart, Samantha J Pitt
Aberrant Zn2+-homeostasis is associated with dysregulated intracellular Ca2+ release resulting in chronic heart failure. In the failing heart, a small population of cardiac ryanodine receptors (RyR2) display sub-conductance state gating leading to Ca2+ leakage from sarcoplasmic reticulum (SR) stores, which impairs cardiac contractility. Previous evidence suggests contribution of RyR2-independent Ca2+ leakage through an uncharacterized mechanism. We sought to examine the role of Zn2+ in shaping intracellular Ca2+ release in cardiac muscle...
June 19, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28620067/allele-specific-silencing-of-mutant-mrna-rescues-ultrastructural-and-arrhythmic-phenotype-in-mice-carriers-of-the-r4496c-mutation-in-the-ryanodine-receptor-gene-ryr2
#5
Rossana Bongianino, Marco Denegri, Andrea Mazzanti, Francesco Lodola, Alessandra Vollero, Simona Boncompagni, Silvia Fasciano, Giulia Rizzo, Damiano Mangione, Serena Barbaro, Alessia Di Fonso, Carlo Napolitano, Alberto Auricchio, Feliciano Protasi, Silvia G Priori
Rationale: Mutations in the cardiac Ryanodine Receptor gene (RYR2) cause dominant Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT), a leading cause of sudden death in apparently healthy individuals exposed to emotions or physical exercise. Objective: We investigated the efficacy of allele specific silencing by RNA interference to prevent CPVT phenotypical manifestations in our dominant CPVT mice model carriers of the heterozygous mutation R4496C in RYR2Methods and Results: We developed an in vitro mRNA and protein-based assays to screen multiple siRNAs for their ability to selectively silence mutant RYR2-R4496C mRNA over the corresponding wild-type (WT) allele...
June 15, 2017: Circulation Research
https://www.readbyqxmd.com/read/28618061/electrical-storm-in-a-patient-with-duchenne-muscular-dystrophy-cardiomyopathy-triggered-by-abrupt-%C3%AE-blocker-interruption
#6
Nikolaos Fragakis, Melani Sotiriadou, Lydia Krexi, Vassilios Vassilikos
We present a case of a young man with Duchenne muscular dystrophy cardiomyopathy (DMDC) having an implantable cardioverter defibrillator for secondary prevention, who presented with electrical storm shortly after β-blocker interruption. The patient was stabilized and remained free of ventricular arrhythmias soon after reinitiating b-adrenoreceptor antagonists. The present case highlights the importance of sympathetic blockage in patients with DMDC due to existing pathophysiology of excess diastolic Ca(2+) leak from sarcoplasmic reticulum as a result of ryanodine receptor dysfunction...
June 15, 2017: Annals of Noninvasive Electrocardiology
https://www.readbyqxmd.com/read/28617952/systolic-ca-2-i-regulates-diastolic-levels-in-rat-ventricular-myocytes
#7
R Sankaranarayanan, K Kistamas, D J Greensmith, L A Venetucci, D A Eisner
[Ca(2+) ]i must be low enough in diastole so that the ventricle is relaxed and can refill with blood. Interference with this will impair relaxation. The factors responsible for regulation of diastolic [Ca(2+) ]i , in particular the relative roles of the sarcoplasmic reticulum (SR) and surface membrane are unclear. We investigated the effects on diastolic [Ca(2+) ]i that result from the changes of Ca cycling known to occur in heart failure. Experiments were performed using Fluo-3 in voltage-clamped rat ventricular myocytes...
June 15, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28612156/reduction-of-sr-ca-2-leak-and-arrhythmogenic-cellular-correlates-by-smp-114-a-novel-camkii-inhibitor-with-oral-bioavailability
#8
Stefan Neef, Christian Mann, Anne Zwenger, Nataliya Dybkova, Lars S Maier
Sarcoplasmic reticulum (SR) Ca(2+) leak induced by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is centrally involved in atrial and ventricular arrhythmogenesis as well as heart failure remodeling. Consequently, treating SR Ca(2+) leak has been proposed as a novel therapeutic paradigm, but compounds for use in humans are lacking. SMP-114 ("Rimacalib") is a novel, orally available CaMKII inhibitor developed for human use that has already entered clinical phase II trials to treat rheumatoid arthritis...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28611207/adult-ventricular-myocytes-segregate-kcnq1-and-kcne1-to-keep-the-iks-amplitude-in-check-until-when-larger-iks-is-needed
#9
Min Jiang, Yuhong Wang, Gea-Ny Tseng
BACKGROUND: KCNQ1 and KCNE1 assemble to form the slow delayed rectifier (IKs) channel critical for shortening ventricular action potentials during high β-adrenergic tone. However, too much IKs under basal conditions poses an arrhythmogenic risk. Our objective is to understand how adult ventricular myocytes regulate the IKs amplitudes under basal conditions and in response to stress. METHODS AND RESULTS: We express fluorescently tagged KCNQ1 and KCNE1 in adult ventricular myocytes and follow their biogenesis and trafficking paths...
June 2017: Circulation. Arrhythmia and Electrophysiology
https://www.readbyqxmd.com/read/28596578/transgenic-overexpression-of-gtp-cyclohydrolase-1-in-cardiomyocytes-ameliorates-post-infarction-cardiac-remodeling
#10
Yanan Liu, Shelley L Baumgardt, Juan Fang, Yang Shi, Shigang Qiao, Zeljko J Bosnjak, Jeannette Vásquez-Vivar, Zhengyuan Xia, David C Warltier, Judy R Kersten, Zhi-Dong Ge
GTP cyclohydrolase 1 (GCH1) and its product tetrahydrobiopterin play crucial roles in cardiovascular health and disease, yet the exact regulation and role of GCH1 in adverse cardiac remodeling after myocardial infarction are still enigmatic. Here we report that cardiac GCH1 is degraded in remodeled hearts after myocardial infarction, concomitant with increases in the thickness of interventricular septum, interstitial fibrosis, and phosphorylated p38 mitogen-activated protein kinase and decreases in left ventricular anterior wall thickness, cardiac contractility, tetrahydrobiopterin, the dimers of nitric oxide synthase, sarcoplasmic reticulum Ca(2+) release, and the expression of sarcoplasmic reticulum Ca(2+) handling proteins...
June 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28595923/microstructural-and-ultrastructural-changes-in-the-muscle-cells-of-the-oriental-armyworm-mythimna-separata-walker-lepidoptera-noctuidae-on-treatment-with-wilforine
#11
Shujie Ma, Lin Liu, Zhiqing Ma, Xing Zhang
This study investigated the mode of action of wilforine, an alkaloid with insecticidal properties, extracted from Tripterygium wilfordii Hook f., on the microstructure and ultrastructure of the muscle cells of larvae and adults of the oriental armyworm Mythimna separata Walker. The bioassay results showed that wilforine had oral toxicity against both M. separata larvae (LC50=63μg/mL) and adults (LC50=36μg/mL). The typical toxicity sign was paralysis leading to death. Both light and electron microscope observations revealed that damage to the muscle cells increased with poisoning time in larvae and adults treated with the LC80 dose of wilforine...
June 2017: Pesticide Biochemistry and Physiology
https://www.readbyqxmd.com/read/28595547/beneficial-effects-of-n-acetylcysteine-and-n-mercaptopropionylglycine-on-ischemia-reperfusion-injury-in-the-heart
#12
Monika Bartekova, Miroslav Barancik, Kristina Ferenczyova, Narajan S Dhalla
Ischemia-reperfusion (I/R) injury of the heart as a consequence of myocardial infarction or cardiac surgery represents a serious clinical problem. One of the most prominent mechanisms of I/R injury is the development of oxidative stress in the heart. In this regard, I/R has been shown to enhance the production of reactive oxygen/nitrogen species in the heart which lead to the imbalance between the pro-oxidants and antioxidant capacities of the endogenous radical-scavenging systems. Accordingly, increasing the antioxidant capacity of the heart by the administration of exogenous antioxidants is considered beneficial for the heart exposed to I/R...
June 8, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28595501/astragaloside-iv-inhibits-membrane-ca-formula-see-text-current-but-enhances-sarcoplasmic-reticulum-ca-formula-see-text-release
#13
Mei-Mi Zhao, Wen-Wen Lian, Zhuo Li, Dong-Xue Shao, Si-Chong Chen, Xue-Fei Sun, Hui-Yuan Hu, Rui Feng, Feng Guo, Li-Ying Hao
Astragaloside IV (AS-IV) is one of the active ingredients in Astragalus membrananceus (Huangqi), a traditional Chinese medicine. The present study investigated the effects of AS-IV on Ca[Formula: see text] handling in cardiac myocytes to elucidate its possible mechanism in the treatment of cardiac disease. The results showed that AS-IV at 1 and 10[Formula: see text][Formula: see text]M reduced KCl-induced [Ca[Formula: see text]]i increase ([Formula: see text] from 1.33[Formula: see text][Formula: see text][Formula: see text]0...
2017: American Journal of Chinese Medicine
https://www.readbyqxmd.com/read/28593034/nanospan-an-alternatively-spliced-isoform-of-sarcospan-localizes-to-the-sarcoplasmic-reticulum-in-skeletal-muscle-and-is-absent-in-limb-girdle-muscular-dystrophy-2f
#14
Angela K Peter, Gaynor Miller, Joana Capote, Marino DiFranco, Alhondra Solares-Pérez, Emily L Wang, Jim Heighway, Ramón M Coral-Vázquez, Julio Vergara, Rachelle H Crosbie-Watson
BACKGROUND: Sarcospan (SSPN) is a transmembrane protein that interacts with the sarcoglycans (SGs) to form a tight subcomplex within the dystrophin-glycoprotein complex that spans the sarcolemma and interacts with laminin in the extracellular matrix. Overexpression of SSPN ameliorates Duchenne muscular dystrophy in murine models. METHODS: Standard cloning approaches were used to identify nanospan, and nanospan-specific polyclonal antibodies were generated and validated...
2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28592415/role-of-stim1-in-hypertrophy-related-contractile-dysfunction
#15
Constantine D Troupes, Markus Wallner, Giulia Borghetti, Chen Zhang, Sadia Mohsin, Dirk von Lewinski, Remus M Berretta, Hajime Kubo, Xiongwen Chen, Jonathan Soboloff, Steven R Houser
Rationale: Pathological increases in cardiac afterload result in myocyte hypertrophy with changes in myocyte electrical and mechanical phenotype. Remodeling of contractile and signaling Ca(2+) occurs in pathological hypertrophy and is central to myocyte remodeling. Stromal Interaction Molecule 1 (STIM1) regulates Ca(2+) signaling in many cell types by sensing low endoplasmic reticular Ca(2+) levels and then coupling to plasma membrane Orai channels to induce a Ca(2+) influx pathway. Previous reports suggest that STIM1 may play a role in cardiac hypertrophy but its role in electrical and mechanical phenotypic alterations are not well understood...
June 7, 2017: Circulation Research
https://www.readbyqxmd.com/read/28590578/acute-inhibitory-effect-of-alpha-mangostin-on-sarcoplasmic-reticulum-calcium-atpase-and-myocardial-relaxation
#16
Sukanya Phungphong, Anusak Kijtawornrat, Pieter P de Tombe, Jonggonnee Wattanapermpool, Tepmanas Bupha-Intr, Sunit Suksamrarn
The benefits of α-mangostin for various tissues have been reported, but its effect on the heart has not been clarified. This study aimed to evaluate the effects of α-mangostin on cardiac function. Using a cardiac sarcoplasmic reticulum (SR) membrane preparation, α-mangostin inhibited SR Ca(2+) -ATPase activity in a dose-dependent manner (IC50 of 6.47 ± 0.7 μM). Its suppressive effect was specific to SR Ca(2+) -ATPase but not to myofibrillar Ca(2+) -ATPase. Using isolated cardiomyocytes, 50 μM of α-mangostin significantly increased the duration of cell relengthening and increased the duration of Ca(2+) transient decay, suggesting altered myocyte relaxation...
June 7, 2017: Journal of Biochemical and Molecular Toxicology
https://www.readbyqxmd.com/read/28587810/subcellular-localization-of-na-k-atpase-isoforms-in-ventricular-myocytes
#17
Garrick K Yuen, Samuel Galice, Donald M Bers
The sodium/potassium ATPase (NKA) is essential for establishing the normal intracellular [Na(+)] and [K(+)] and transmembrane gradients that are essential for many cellular functions, including cardiac electrophysiology and contractility. Different NKA isoforms exhibit differential expression levels, cellular localization, and function in different tissues and species. Prior work has indicated that the NKA-α1 isoform is quantitatively predominant in cardiac myocytes, but that the α2 isoform is preferentially concentrated in the transverse tubules (TT), possibly at junctions with the sarcoplasmic reticulum (SR) where α2 may preferentially modulate cardiac contractility...
June 3, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28587652/nanospan-an-alternatively-spliced-isoform-of-sarcospan-localizes-to-the-sarcoplasmic-reticulum-in-skeletal-muscle-and-is-absent-in-limb-girdle-muscular-dystrophy-2f
#18
Angela K Peter, Gaynor Miller, Joana Capote, Marino DiFranco, Alhondra Solares-Pérez, Emily L Wang, Jim Heighway, Ramón M Coral-Vázquez, Julio Vergara, Rachelle H Crosbie-Watson
BACKGROUND: Sarcospan (SSPN) is a transmembrane protein that interacts with the sarcoglycans (SGs) to form a tight subcomplex within the dystrophin-glycoprotein complex that spans the sarcolemma and interacts with laminin in the extracellular matrix. Overexpression of SSPN ameliorates Duchenne muscular dystrophy in murine models. METHODS: Standard cloning approaches were used to identify nanospan, and nanospan-specific polyclonal antibodies were generated and validated...
June 6, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28587334/effect-of-acute-peritonitis-on-rocuronium-induced-intraperitoneal-pressure-reduction-and-the-uptake-function-of-the-sarcoplasmic-reticulum
#19
Jian-You Zhang, Yuan Gong, Mei-Rong Yang, Jin Wu, Shi-Tong Li
Previous studies have reported the incomplete relaxation effect of neuromuscular blockers on skeletal muscles in acute peritonitis (AP) and other inflammatory processes; however, the underlying mechanisms responsible for this effect have not yet been satisfactorily identified. The impaired removal of cytosolic Ca(2+) through sarcoendoplasmic Ca(2+)-ATPase (SERCA) and defects in sarcoplasmic reticulum (SR) Ca(2+) uptake are the major contributing factors to diastolic dysfunction. Previous studies on the effects of neuromuscular blockers have primarily focused on neuromuscular transmission...
June 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28584051/ion-pulling-simulations-provide-insights-into-the-mechanisms-of-channel-opening-of-the-skeletal-muscle-ryanodine-receptor
#20
David D Mowrey, Le Xu, Yingwu Mei, Daniel A Pasek, Gerhard Meissner, Nikolay V Dokholyan
The type 1 ryanodine receptor (RyR1) mediates Ca(2+) release from the sarcoplasmic reticulum to initiate skeletal muscle contraction and is associated with muscle diseases, malignant hyperthermia, and central core disease. To better understand RyR1 channel function, we investigated the molecular mechanisms of channel gating and ion permeation. An adequate model of channel gating requires accurate, high-resolution models of both open and closed states of the channel. To this end, we generated an open-channel RyR1 model using molecular simulations to pull Ca(2+) through the pore constriction site of a closed-channel RyR1 structure determined at 3...
June 5, 2017: Journal of Biological Chemistry
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