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https://www.readbyqxmd.com/read/28439258/diabetic-cardiomyopathy-an-immunometabolic-perspective
#1
REVIEW
Paras K Mishra, Wei Ying, Shyam Sundar Nandi, Gautam K Bandyopadhyay, Kaushik K Patel, Sushil K Mahata
The heart possesses a remarkable inherent capability to adapt itself to a wide array of genetic and extrinsic factors to maintain contractile function. Failure to sustain its compensatory responses results in cardiac dysfunction, leading to cardiomyopathy. Diabetic cardiomyopathy (DCM) is characterized by left ventricular hypertrophy and reduced diastolic function, with or without concurrent systolic dysfunction in the absence of hypertension and coronary artery disease. Changes in substrate metabolism, oxidative stress, endoplasmic reticulum stress, formation of extracellular matrix proteins, and advanced glycation end products constitute the early stage in DCM...
2017: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/28438761/improved-skeletal-muscle-ca-2-regulation-in-vivo-following-contractions-in-mice-overexpressing-pgc-1%C3%AE
#2
Hiroaki Eshima, Shinji Miura, Nanami Senoo, Koji Hatakeyama, David C Poole, Yutaka Kano
In skeletal muscle, resting intracellular Ca(2+) concentration ([Ca(2+)]i) homeostasis is exquisitely regulated by Ca(2+) transport across the sarcolemmal, mitochondrial and sarcoplasmic reticulum (SR) membranes. Of these three systems, the relative importance of the mitochondria in [Ca(2+)]i regulation remains poorly understood in in vivo skeletal muscle. We tested the hypothesis that the capacity for Ca(2+) uptake by mitochondria is a primary factor in determining [Ca(2+)]i regulation in muscle at rest and following contractions...
April 24, 2017: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
https://www.readbyqxmd.com/read/28424631/mechanisms-underlying-the-emergence-of-post-acidosis-arrhythmia-at-the-tissue-level-a-theoretical-study
#3
Jieyun Bai, Renli Yin, Kuanquan Wang, Henggui Zhang
Acidosis has complex electrophysiological effects, which are associated with a high recurrence of ventricular arrhythmias. Through multi-scale cardiac computer modeling, this study investigated the mechanisms underlying the emergence of post-acidosis arrhythmia at the tissue level. In simulations, ten Tusscher-Panfilov ventricular model was modified to incorporate various data on acidosis-induced alterations of cellular electrophysiology and intercellular electrical coupling. The single cell models were incorporated into multicellular one-dimensional (1D) fiber and 2D sheet tissue models...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28410273/up-regulation-of-intracellular-calcium-handling-underlies-the-recovery-of-endotoxemic-cardiomyopathy-in-mice
#4
Justin C Morse, Joanne Huang, Natasha Khona, Edward J Miller, Deborah A Siwik, Wilson S Colucci, Ion A Hobai
BACKGROUND: In surviving patients, sepsis-induced cardiomyopathy is spontaneously reversible. In the absence of any experimental data, it is generally thought that cardiac recovery in sepsis simply follows the remission of systemic inflammation. Here the authors aimed to identify the myocardial mechanisms underlying cardiac recovery in endotoxemic mice. METHODS: Male C57BL/6 mice were challenged with lipopolysaccharide (7 μg/g, intraperitoneally) and followed for 12 days...
April 14, 2017: Anesthesiology
https://www.readbyqxmd.com/read/28324061/progesterone-protects-against-bisphenol-a-induced-arrhythmias-in-female-rat-cardiac-myocytes-via-rapid-signaling
#5
Jianyong Ma, Kui Hong, Hong-Sheng Wang
Bisphenol A (BPA) is an estrogenic endocrine-disrupting chemical (EDC) that has a range of potential adverse health effects. Previously we showed that acute exposure to BPA promoted arrhythmias in female rat hearts through estrogen receptor rapid signaling. Progesterone (P4) and estrogen have antagonistic or complementary actions in a number of tissues and systems. In the current study, we examined the influence and possible protective effect of P4 on the rapid cardiac actions of BPA in female rat cardiac myocytes...
April 1, 2017: Endocrinology
https://www.readbyqxmd.com/read/28321411/different-densities-of-na-ca-exchange-current-in-t-tubular-and-surface-membranes-and-their-impact-on-cellular-activity-in-a-model-of-rat-ventricular-cardiomyocyte
#6
M Pásek, J Šimurda, G Christé
The ratio of densities of Na-Ca exchanger current (INaCa) in the t-tubular and surface membranes (INaCa-ratio) computed from the values of INaCa and membrane capacitances (Cm) measured in adult rat ventricular cardiomyocytes before and after detubulation ranges between 1.7 and 25 (potentially even 40). Variations of action potential waveform and of calcium turnover within this span of the INaCa-ratio were simulated employing previously developed model of rat ventricular cell incorporating separate description of ion transport systems in the t-tubular and surface membranes...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28292875/in-vivo-ca-2-dynamics-induced-by-ca-2-injection-in-individual-rat-skeletal-muscle-fibers
#7
Mario Wakizaka, Hiroaki Eshima, Yoshinori Tanaka, Hideki Shirakawa, David C Poole, Yutaka Kano
In contrast to cardiomyocytes, store overload-induced calcium ion (Ca(2+)) release (SOICR) is not considered to constitute a primary Ca(2+) releasing system from the sarcoplasmic reticulum (SR) in skeletal muscle myocytes. In the latter, voltage-induced Ca(2+) release (VICR) is regarded as the dominant mechanism facilitating contractions. Any role of the SOICR in the regulation of cytoplasmic Ca(2+) concentration ([Ca(2+)]i) and its dynamics in skeletal muscle in vivo remains poorly understood. By means of in vivo single fiber Ca(2+) microinjections combined with bioimaging techniques, we tested the hypothesis that the [Ca(2+)]i dynamics following Ca(2+) injection would be amplified and fiber contraction facilitated by SOICR...
March 2017: Physiological Reports
https://www.readbyqxmd.com/read/28257761/membrane-potential-determines-calcium-alternans-through-modulation-of-sr-ca-2-load-and-l-type-ca-2-current
#8
Giedrius Kanaporis, Lothar A Blatter
Alternans is a risk factor for cardiac arrhythmia, including atrial fibrillation. At the cellular level alternans is observed as beat-to-beat alternations in contraction, action potential (AP) morphology and magnitude of the Ca(2+) transient (CaT). It is widely accepted that the bi-directional interplay between membrane voltage and Ca(2+) is crucial for the development of alternans, however recently the attention has shifted to instabilities in cellular Ca(2+) handling, while the role of AP alternation remains poorly understood...
April 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28169003/increased-calcium-leak-associated-with-reduced-calsequestrin-expression-in-hyperthyroid-cardiomyocytes
#9
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/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...
April 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28143888/divergent-mechanisms-leading-to-signaling-dysfunction-in-embryonic-muscle-by-bisphenol-a-and-tetrabromobisphenol-a
#11
Rui Zhang, Isaac N Pessah
Bisphenol A (BPA) and its brominated derivative tetrabromobisphenol A (TBBPA) are high production volume chemicals used in the manufacture of various consumer products. Although regarded as endocrine disruptors, these chemicals are suspected to exert nongenomic 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 sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase (SERCA)...
April 2017: Molecular Pharmacology
https://www.readbyqxmd.com/read/28131630/the-effect-of-pka-mediated-phosphorylation-of-ryanodine-receptor-on-sr-ca-2-leak-in-ventricular-myocytes
#12
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...
March 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
#13
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/28105734/calcium-calmodulin-dependent-protein-kinase-mediates-the-intracellular-signaling-pathways-of-cardiac-apoptosis-in-mice-with-impaired-glucose-tolerance
#14
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
https://www.readbyqxmd.com/read/28102477/potential-new-mechanisms-of-pro-arrhythmia-in-arrhythmogenic-cardiomyopathy-focus-on-calcium-sensitive-pathways
#15
REVIEW
C J M van Opbergen, M Delmar, T A B van Veen
Arrhythmogenic cardiomyopathy, or its most well-known subform arrhythmogenic right ventricular cardiomyopathy (ARVC), is a cardiac disease mainly characterised by a gradual replacement of the myocardial mass by fibrous and fatty tissue, leading to dilatation of the ventricular wall, arrhythmias and progression towards heart failure. ARVC is commonly regarded as a disease of the intercalated disk in which mutations in desmosomal proteins are an important causative factor. Interestingly, the Dutch founder mutation PLN R14Del has been identified to play an additional, and major, role in ARVC patients within the Netherlands...
March 2017: Netherlands Heart Journal
https://www.readbyqxmd.com/read/27881388/hyperglycemia-induces-defective-ca2-homeostasis-in-cardiomyocytes
#16
Andrea Sorrentino, Giulia Borghetti, Yu Zhou, Antonio Cannata, Marianna Meo, Sergio Signore, Piero Anversa, Annarosa Leri, Polina Goichberg, Khaled Qanud, Jason T Jacobson, Thomas H Hintze, Marcello Rota
Diabetes and other metabolic conditions characterized by elevated blood glucose constitute important risk factors for cardiovascular disease. Hyperglycemia targets myocardial cells rendering ineffective mechanical properties of the heart, but cellular alterations dictating the progressive deterioration of cardiac function with metabolic disorders remain to be clarified. In the current study, we examined the effects of hyperglycemia on cardiac function and myocyte physiology by employing mice with high blood glucose induced by administration of streptozotocin, a compound toxic to insulin-producing β-cells...
January 1, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/27816525/enhanced-nucleoplasmic-ca-2-signaling-in-ventricular-myocytes-from-young-hypertensive-rats
#17
Jelena Plačkić, Sebastian Preissl, Yulia Nikonova, Florentina Pluteanu, Lutz Hein, Jens Kockskämper
Arterial hypertension causes left ventricular (LV) myocyte hypertrophy. Alterations in nuclear Ca(2+) may be involved in regulation of histone acetylation, transcription and hypertrophy. Regulation of nuclear Ca(2+) in hypertension, however, is unknown. Therefore, we elucidated cellular mechanisms underlying nuclear Ca(2+) regulation in LV myocytes from hypertensive versus normotensive rats and evaluated possible consequences for Ca(2+)-dependent regulation of histone acetylation. LV myocytes and myocyte nuclei were isolated from young spontaneously hypertensive rats (SHR) shortly after development of hypertension...
December 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27799555/cardiac-electrical-defects-in-progeroid-mice-and-hutchinson-gilford-progeria-syndrome-patients-with-nuclear-lamina-alterations
#18
José Rivera-Torres, Conrado J Calvo, Anna Llach, Gabriela Guzmán-Martínez, Ricardo Caballero, Cristina González-Gómez, Luis J Jiménez-Borreguero, Juan A Guadix, Fernando G Osorio, Carlos López-Otín, Adela Herraiz-Martínez, Nuria Cabello, Alex Vallmitjana, Raul Benítez, Leslie B Gordon, José Jalife, José M Pérez-Pomares, Juan Tamargo, Eva Delpón, Leif Hove-Madsen, David Filgueiras-Rama, Vicente Andrés
Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disease caused by defective prelamin A processing, leading to nuclear lamina alterations, severe cardiovascular pathology, and premature death. Prelamin A alterations also occur in physiological aging. It remains unknown how defective prelamin A processing affects the cardiac rhythm. We show age-dependent cardiac repolarization abnormalities in HGPS patients that are also present in the Zmpste24(-/-) mouse model of HGPS. Challenge of Zmpste24(-/-) mice with the β-adrenergic agonist isoproterenol did not trigger ventricular arrhythmia but caused bradycardia-related premature ventricular complexes and slow-rate polymorphic ventricular rhythms during recovery...
November 15, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27491078/a-human-pluripotent-stem-cell-model-of-catecholaminergic-polymorphic-ventricular-tachycardia-recapitulates-patient-specific-drug-responses
#19
Marcela K Preininger, Rajneesh Jha, Joshua T Maxwell, Qingling Wu, Monalisa Singh, Bo Wang, Aarti Dalal, Zachary T Mceachin, Wilfried Rossoll, Chadwick M Hales, Peter S Fischbach, Mary B Wagner, Chunhui Xu
Although β-blockers can be used to eliminate stress-induced ventricular arrhythmias in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT), this treatment is unsuccessful in ∼25% of cases. Induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) generated from these patients have potential for use in investigating the phenomenon, but it remains unknown whether they can recapitulate patient-specific drug responses to β-blockers. This study assessed whether the inadequacy of β-blocker therapy in an individual can be observed in vitro using patient-derived CPVT iPSC-CMs...
September 1, 2016: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/27322594/electrophysiological-basis-of-metabolic-syndrome-induced-cardiac-dysfunction
#20
Esma N Okatan, Aysegul Toy Durak, Belma Turan
Myocardial contractility is controlled by intracellular Ca(2+) cycling with the contribution of sarcoplasmic reticulum (SR). In this study, we aimed to investigate the role of altered SR function in defective regulation of intracellular Ca(2+) levels in rats with metabolic syndrome (MetS) induced by a 16-week high-sucrose drinking-water diet. Electric-field stimulated transient intracellular Ca(2+) changes in MetS cardiomyocytes exhibited significantly reduced amplitude (∼30%) and prolonged time courses (2-fold), as well as depressed SR Ca(2+) loading (∼55%) with increased basal Ca(2+) level...
April 12, 2016: Canadian Journal of Physiology and Pharmacology
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