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https://www.readbyqxmd.com/read/28209802/doublet-stimulation-increases-ca-2-binding-to-troponin-c-to-ensure-rapid-force-development-in-skeletal-muscle
#1
Anthony J Bakker, Tanya R Cully, Catherine D Wingate, Christopher J Barclay, Bradley S Launikonis
Fast-twitch skeletal muscle fibers are often exposed to motor neuron double discharges (≥200 Hz), which markedly increase both the rate of contraction and the magnitude of the resulting force responses. However, the mechanism responsible for these effects is poorly understood, likely because of technical limitations in previous studies. In this study, we measured cytosolic Ca(2+) during doublet activation using the low-affinity indicator Mag-Fluo-4 at high temporal resolution and modeled the effects of doublet stimulation on sarcoplasmic reticulum (SR) Ca(2+) release, binding of Ca(2+) to cytosolic buffers, and force enhancement in fast-twitch fibers...
February 16, 2017: Journal of General Physiology
https://www.readbyqxmd.com/read/28209766/glycosylated-chromogranin-a-in-heart-failure-implications-for-processing-and-cardiomyocyte-calcium-homeostasis
#2
Anett Hellebø Ottesen, Cathrine R Carlson, William E Louch, Mai Britt Dahl, Ragnhild A Sandbu, Rune Forstrøm Johansen, Hilde Jarstadmarken, Magnar Bjørås, Arne Didrik Høiseth, Jon Brynildsen, Ivar Sjaastad, Mats Stridsberg, Torbjørn Omland, Geir Christensen, Helge Røsjø
BACKGROUND: Chromogranin A (CgA) levels have previously been found to predict mortality in heart failure (HF), but currently no information is available regarding CgA processing in HF and whether the CgA fragment catestatin (CST) may directly influence cardiomyocyte function. METHODS AND RESULTS: CgA processing was characterized in postinfarction HF mice and in patients with acute HF, and the functional role of CST was explored in experimental models. Myocardial biopsies from HF, but not sham-operated mice, demonstrated high molecular weight CgA bands...
February 2017: Circulation. Heart Failure
https://www.readbyqxmd.com/read/28192519/arachidonic-acid-triggers-ca2-i-increases-in-rat-round-spermatids-by-a-likely-gpr-activation-erk-signalling-and-er-acidic-compartments-ca2-release
#3
Joaquin Paillamanque, Ana Sanchez-Tusie, Emerson M Carmona, Claudia L Treviño, Carolina Sandoval, Francisco Nualart, Nelson Osses, Juan G Reyes
Arachidonic acid (AA), a compound secreted by Sertoli cells (SC) in a FSH-dependent manner, is able to induce the release of Ca2+ from internal stores in round spermatids and pachytene spermatocytes. In this study, the possible site(s) of action of AA in round spermatids, the signalling pathways associated and the intracellular Ca2+ stores targeted by AA-induced signalling were pharmacologically characterized by measuring intracellular Ca2+ using fluorescent Ca2+ probes. Our results suggest that AA acts by interacting with a fatty acid G protein coupled receptor, initiating a G protein signalling cascade that may involve PLA2 and ERK activation, which in turn opens intracellular ryanodine-sensitive channels as well as NAADP-sensitive channels in acidic intracellular Ca2+ stores...
2017: PloS One
https://www.readbyqxmd.com/read/28181698/calcium-uptake-via-mitochondrial-uniporter-contributes-to-palmitic-acid-induced-apoptosis-in-mouse-podocytes
#4
Zeting Yuan, Aili Cao, Hua Liu, Henjiang Guo, Yingjun Zang, Yi Wang, Yunman Wang, Hao Wang, Peihao Yin, Wen Peng
Podocytes are component cells of the glomerular filtration barrier, and their loss by apoptosis is the main cause of proteinuria that leads to diabetic nephropathy (DN). Therefore, insights into podocyte apoptosis mechanism would allow a better understanding of DN pathogenesis and thus help develop adequate therapeutic strategies. Here, we investigated the molecular mechanism of palmitic acid-inhibited cell death in mouse podocytes, and found that palmitic acid increased cell death in a dose- and time-dependent manner...
February 9, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28181690/calcium-mediated-cellular-triggered-activity-in-atrial-fibrillation
#5
Dobromir Dobrev, Xander H T Wehrens
Although atrial fibrillation (AF) is the most commonly encountered cardiac arrhythmia, the basic mechanisms underlying this disorder remain incompletely understood. During the past decade or so, it has become clear that alterations in intracellular Ca(2+) handling may play a role in the pathogenesis of AF. Studies in small and large animal models, as well as atrial samples from patients with different forms of AF have implicated ryanodine receptor type 2 (RyR2) dysfunction and enhanced spontaneous Ca(2+) release events from the sarcoplasmic reticulum (SR) as a potential cause of proarrhythmic cellular ectopic (triggered) activity in AF...
February 9, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28181072/interactions-of-mitochondria-metabolism-and-calcium-regulation-in-alzheimer-s-disease-a-calcinist-point-of-view
#6
Gary E Gibson, Ankita Thakkar
Decades of research suggest that alterations in calcium are central to the pathophysiology of Alzheimer's Disease (AD). Highly reproducible changes in calcium dynamics occur in cells from patients with both genetic and non-genetic forms of AD relative to controls. The most robust change is an exaggerated release of calcium from internal stores. Detailed analysis of these changes in animal and cell models of the AD-causing presenilin mutations reveal robust changes in ryanodine receptors, inositol tris-phosphate receptors, calcium leak channels and store activated calcium entry...
February 8, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28179209/administration-of-anabolic-steroid-during-adolescence-induces-long-term-cardiac-hypertrophy-and-increases-susceptibility-to-ischemia-reperfusion-injury-in-adult-wistar-rats
#7
Fernando de Azevedo Cruz Seara, Raiana Andrade Quintanilha Barbosa, Dahienne Ferreira de Oliveira, Diorney Luiz Souza Gran da Silva, Adriana Bastos Carvalho, Andrea Claudia Freitas Ferreira, José Hamilton Matheus Nascimento, Emerson Lopes Olivares
Chronic administration of anabolic androgenic steroids (AAS) in adult rats results in cardiac hypertrophy and increased susceptibility to myocardial ischemia/reperfusion (IR) injury. Molecular analyses demonstrated that hyperactivation of type 1 angiotensin II (AT1) receptor mediates cardiac hypertrophy induced by AAS and also induces down-regulation of myocardial ATP-sensitive potassium channel (KATP), resulting in loss of exercise-induced cardioprotection. Exposure to AAS during adolescence promoted long-term cardiovascular dysfunctions, such as dysautonomia...
February 5, 2017: Journal of Steroid Biochemistry and Molecular Biology
https://www.readbyqxmd.com/read/28169003/increased-calcium-leak-associated-with-reduced-calsequestrin-expression-in-hyperthyroid-cardiomyocytes
#8
David R de Alba-Aguayo, Natalia Pavón, Martha Mercado-Morales, Miyamin Miranda-Saturnino, Mavil López-Casamichana, Agustin Guerrero-Hernández, Angelica Rueda
INTRODUCTION: Calcium (Ca(2+)) leak during cardiac diastole is chiefly mediated by intracellular Ca(2+) channel/Ryanodine Receptors. Increased diastolic Ca(2+) leak has been proposed as the mechanism underlying the appearance of hereditary arrhythmias. However, little is known about alterations in diastolic Ca(2+) leak and the specific roles played by key intracellular Ca(2+)-handling proteins in hyperthyroidism, a known arrhythmogenic condition. AIM: We sought to determine whether there were modifications in diastolic Ca(2+) leak, based on the recording of Ca(2+) sparks and Ca(2+) waves; we also investigated changes in the expression and activity of key Ca(2+) handling proteins, including ryanodine receptors, Sarco-Endoplasmic Reticulum Ca(2+) ATPase pump and calsequestrin in isolated left-ventricular cardiomyocytes isolated from hyperthyroid rats...
January 23, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28168961/the-amyloid-precursor-protein-intracellular-domain-is-an-effector-molecule-of-metaplasticity
#9
Emilie Trillaud-Doppia, Jannic Boehm
BACKGROUND: Human studies and mouse models of Alzheimer's disease suggest that the amyloid precursor protein (APP) can cause changes in synaptic plasticity and is contributing to the memory deficits seen in Alzheimer's disease. While most of these studies attribute these changes to the APP cleavage product Aβ, in recent years it became apparent that the APP intracellular domain (APP-ICD) might play a role in regulating synaptic plasticity. METHODS: To separate the effects of APP-ICD on synaptic plasticity from Aβ-dependent effects, we created a chimeric APP in which the Aβ domain is exchanged for its homologous domain from the amyloid precursor-like protein 2...
December 22, 2016: Biological Psychiatry
https://www.readbyqxmd.com/read/28159581/recombinant-expression-of-intrepicalcin-from-the-scorpion-vaejovis-intrepidus-and-its-effect-on-skeletal-ryanodine-receptors
#10
Leonel Vargas-Jaimes, Liang Xiao, Jing Zhang, Lourival D Possani, Héctor H Valdivia, Verónica Quintero-Hernández
BACKGROUND: Scorpion venoms contain toxins that modulate ionic channels, among which are the calcins, a small group of short, basic peptides with an Inhibitor Cystine Knot (ICK) motif that target calcium release channels/ryanodine receptors (RyRs) with high affinity and selectivity. Here we describe the heterologous expression of Intrepicalcin, identified by transcriptomic analysis of venomous glands from Vaejovis intrepidus. METHODS: Recombinant Intrepicalcin was obtained in Escherichia coli BL21-DE3 (periplasm) by fusing the Intrepicalcin gene to sequences coding for signal-peptide, thioredoxin, His-tag and enterokinase cleavage site...
January 31, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28158491/functional-local-cross-talk-of-inositol-1-4-5-trisphosphate-receptor-and-ryanodine-receptor-dependent-ca2-release-in-atrial-cardiomyocytes
#11
Marcel Wullschleger, Joaquim Blanch, Marcel Egger
No abstract text is available yet for this article.
February 2, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28149035/chlorantraniliprole-an-unusual-insecticide-poisoning-in-humans
#12
Ajay Kumar Mishra, Vignesh Kumar Chandiraseharan, Nisha Jose, Thambu David Sudarsanam
A 26-year-old female presented with deliberate self-harm using chlorantraniliprole, an unknown substance in human toxicology. She developed symptomatic Mobitz Type I atrioventricular block during observation, for which a temporary pacemaker was inserted. She reverted to sinus rhythm after 48 h and was discharged. Although claimed to be nontoxic to humans, chlorantraniliprole, an insecticide, could cause conduction defects by activating ryanodine receptors. To the best of our knowledge, this is the first case of chlorantraniliprole poisoning reported in the medical literature...
December 2016: Indian Journal of Critical Care Medicine
https://www.readbyqxmd.com/read/28143888/divergent-mechanisms-leading-to-signaling-dysfunction-in-embryonic-muscle-by-bisphenol-a-and-tetrabromobisphenol-a
#13
Rui Zhang, Isaac N Pessah
Bisphenol A (BPA) and its brominated derivative tetrabromobisphenol A (TBBPA) are high production volume chemicals utilized in the manufacture of various consumer products. Although regarded as endocrine disruptors, these chemicals are suspected to exert non-genomic actions on muscle function that are not well understood. Using skeletal muscle microsomes, we examined the effects of BPA and TBBPA on ryanodine receptor type 1 (RyR1), dihydropyridine receptor (DHPR), and sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA)...
January 31, 2017: Molecular Pharmacology
https://www.readbyqxmd.com/read/28131631/ryanodine-receptor-modification-and-regulation-by-intracellular-ca-2-and-mg-2-in-healthy-and-failing-human-hearts
#14
K Walweel, P Molenaar, M S Imtiaz, A Denniss, C Dos Remedios, D F van Helden, A F Dulhunty, D R Laver, N A Beard
RATIONALE: Heart failure is a multimodal disorder, of which disrupted Ca(2+) homeostasis is a hallmark. Central to Ca(2+) homeostasis is the major cardiac Ca(2+) release channel - the ryanodine receptor (RyR2) - whose activity is influenced by associated proteins, covalent modification and by Ca(2+) and Mg(2+). That RyR2 is remodelled and its function disturbed in heart failure is well recognized, but poorly understood. OBJECTIVE: To assess Ca(2+) and Mg(2+) regulation of RyR2 from left ventricles of healthy, cystic fibrosis and failing hearts, and to correlate these functional changes with RyR2 modifications and remodelling...
January 25, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28131630/the-effect-of-pka-mediated-phosphorylation-of-ryanodine-receptor-on-sr-ca-2-leak-in-ventricular-myocytes
#15
Elisa Bovo, Sabine Huke, Lothar A Blatter, Aleksey V Zima
Functional impact of cardiac ryanodine receptor (type 2 RyR or RyR2) phosphorylation by protein kinase A (PKA) remains highly controversial. In this study, we characterized a functional link between PKA-mediated RyR2 phosphorylation level and sarcoplasmic reticulum (SR) Ca(2+) release and leak in permeabilized rabbit ventricular myocytes. Changes in cytosolic [Ca(2+)] and intra-SR [Ca(2+)]SR were measured with Fluo-4 and Fluo-5N, respectively. Changes in RyR2 phosphorylation at two PKA sites, serine-2031 and -2809, were measured with phospho-specific antibodies...
January 25, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28126160/role-of-nod1-in-heart-failure-progression-via-regulation-of-ca-2-handling
#16
Almudena Val-Blasco, María Jose G M Piedras, Gema Ruiz-Hurtado, Natalia Suarez, Patricia Prieto, Silvia Gonzalez-Ramos, Nieves Gómez-Hurtado, Carmen Delgado, Laetitia Pereira, Gemma Benito, Carlos Zaragoza, Nieves Domenech, María Generosa Crespo-Leiro, Daniel Vasquez-Echeverri, Gabriel Nuñez, Eduardo Lopez-Collazo, Lisardo Boscá, María Fernández-Velasco
BACKGROUND: Heart failure (HF) is a complex syndrome associated with a maladaptive innate immune system response that leads to deleterious cardiac remodeling. However, the underlying mechanisms of this syndrome are poorly understood. Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) is a newly recognized innate immune sensor involved in cardiovascular diseases. OBJECTIVES: This study evaluated the role of NOD1 in HF progression. METHODS: NOD1 was examined in human failing myocardium and in a post-myocardial infarction (PMI) HF model evaluated in wild-type (wt-PMI) and Nod1(-/-) mice (Nod1(-/-)-PMI)...
January 31, 2017: Journal of the American College of Cardiology
https://www.readbyqxmd.com/read/28122214/importance-of-altered-levels-of-serca-ip3r-and-ryr-in-vascular-smooth-muscle-cell
#17
Jaijus Pallippadan Johny, Michael J Plank, Tim David
Calcium cycling between the sarcoplasmic reticulum (SR) and the cytosol via the sarco-/endoplasmic reticulum Ca-ATPase (SERCA) pump, inositol-1,4,5-triphosphate receptor (IP3R), and Ryanodine receptor (RyR), plays a major role in agonist-induced intracellular calcium ([Ca(2+)]cyt) dynamics in vascular smooth muscle cells (VSMC). Levels of these calcium handling proteins in SR get altered under disease conditions. We have developed a mathematical model to understand the significance of altered levels of SERCA, IP3R, and RyR on the intracellular calcium dynamics of VSMC and to understand how variation in protein levels that arise due to diabetes contribute to different VSMC behavior and thus vascular disease...
January 24, 2017: Biophysical Journal
https://www.readbyqxmd.com/read/28115480/sexual-dimorphism-in-a-reciprocal-interaction-of-ryanodine-and-ip3-receptors-in-the-induction-of-hyperalgesic-priming
#18
Eugen V Khomula, Luiz F Ferrari, Dionéia Araldi, Jon D Levine
: Hyperalgesic priming, a model of pain chronification in the rat is mediated by ryanodine receptor-dependent calcium release. While ryanodine induces priming in both sexes, females are 5-orders of magnitude more sensitive, by an estrogen receptor alpha (EsRα)-dependent mechanism. An inositol 1,4,5-triphosphate (IP3) receptor inhibitor prevented the induction of priming by ryanodine. For IP3 induced priming, females were also more sensitive. IP3-induced priming was prevented by pre-treatment with inhibitors of the sarco-endoplasmic reticulum calcium ATPase and ryanodine receptor...
January 23, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28111173/cardiac-expression-of-ryanodine-receptor-subtype-3-a-strategic-component-in-the-intracellular-ca-2-release-system-of-purkinje-fibers-in-large-mammalian-heart
#19
Rebecca E Daniels, Kazi T Haq, Lawson S Miller, Elizabeth W Chia, Masahito Miura, Vincenzo Sorrentino, John J McGuire, Bruno D Stuyvers
BACKGROUND: Three distinct Ca(2+) release channels were identified in dog P-cells: the ryanodine receptor subtype 2 (RyR2) was detected throughout the cell, while the ryanodine receptor subtype 3 (RyR3) and inositol phosphate sensitive Ca(2+) release channel (InsP3R) were found in the cell periphery. How each of these channels contributes to the Ca(2+) cycling of P-cells is unclear. Recent modeling of Ca(2+) mobilization in P-cells suggested that Ca(2+) sensitivity of Ca(2+)induced Ca(2+)release (CICR) was larger at the P-cell periphery...
January 20, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28105734/calcium-calmodulin-dependent-protein-kinase-mediates-the-intracellular-signaling-pathways-of-cardiac-apoptosis-in-mice-with-impaired-glucose-tolerance
#20
Marilen Federico, Enrique L Portiansky, Leandro Sommese, Francisco J Alvarado, Paula G Blanco, Carolina N Zanuzzi, John Dedman, Marcia Kaetzel, Xander H T Wehrens, Alicia Mattiazzi, Julieta Palomeque
Background The impact of cardiac apoptosis in pre-diabetic stages of diabetic cardiomyopathy is unknown. We described that myocytes from fructose-rich diet (FRD) animals exhibit arrhythmias produced by exacerbated Ca(2+) /calmodulin-protein kinase (CaMKII) activity, ryanodine receptors (RyR2) phosphorylation and sarcoplasmic reticulum (SR) Ca(2+) leak. We tested the hypothesis that this mechanism also underlies cardiac apoptosis in pre-diabetes. Methods and Results We generated a pre-diabetic model in mice fed with FRD...
January 20, 2017: Journal of Physiology
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