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Journal of Molecular and Cellular Cardiology

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https://www.readbyqxmd.com/read/29037982/early-effects-of-epac-depend-on-the-fine-tuning-of-the-sarcoplasmic-reticulum-ca-2-handling-in-cardiomyocytes
#1
N Lezcano, J I E Mariángelo, L Vittone, X H T Wehrens, M Said, C Mundiña-Weilenmann
In cardiac muscle, signaling through cAMP governs many fundamental cellular functions, including contractility, relaxation and automatism. cAMP cascade leads to the activation of the classic protein kinase A but also to the stimulation of the recently discovered exchange protein directly activated by cAMP (Epac). The role of Epac in the regulation of intracellular Ca(2+) homeostasis and contractility in cardiac myocytes is still matter of debate. In this study we showed that the selective Epac activator, 8-(4-chloro-phenylthio)-2'-O-methyladenosine-3', 5'-cyclic monophosphate (8-CPT), produced a positive inotropic effect when adult rat cardiac myocytes were stabilized at low [Ca(2+)]o (0...
October 13, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29032102/regulation-of-ca-2-signaling-by-acute-hypoxia-and-acidosis-in-rat-neonatal-cardiomyocytes
#2
José-Carlos Fernández-Morales, Martin Morad
Ischemic heart disease is an arrhythmogenic condition, accompanied by hypoxia, acidosis, and impaired Ca(2+) signaling. Here we report on effects of acute hypoxia and acidification in rat neonatal cardiomyocytes cultures. RESULTS: Two populations of neonatal cardiomyocyte were identified based on inactivation kinetics of L-type ICa: rapidly-inactivating ICa (τ~20ms) myocytes (prevalent in 3-4-day cultures), and slow-inactivating ICa (τ≥40ms) myocytes (dominant in 7-day cultures). Acute hypoxia (pO2<5mmHg for 50-100s) suppressed ICa reversibly in both cell-types to different extent and with different kinetics...
October 11, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29024690/sodium-channel-current-loss-of-function-in-induced-pluripotent-stem-cell-derived-cardiomyocytes-from-a-brugada-syndrome-patient
#3
Elisabet Selga, Franziska Sendfeld, Rebecca Martinez-Moreno, Claire N Medine, Olga Tura-Ceide, Sir Ian Wilmut, Guillermo J Pérez, Fabiana S Scornik, Ramon Brugada, Nicholas L Mills
Brugada syndrome predisposes to sudden death due to disruption of normal cardiac ion channel function, yet our understanding of the underlying cellular mechanisms is incomplete. Commonly used heterologous expression models lack many characteristics of native cardiomyocytes and, in particular, the individual genetic background of a patient. Patient-specific induced pluripotent stem (iPS) cell-derived cardiomyocytes (iPS-CM) may uncover cellular phenotypical characteristics not observed in heterologous models...
October 9, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28993153/tfeb-activation-protects-against-cardiac-proteotoxicity-via-increasing-autophagic-flux
#4
Bo Pan, Hanming Zhang, Taixing Cui, Xuejun Wang
Insufficient lysosomal removal of autophagic cargoes in cardiomyocytes has been suggested as a main cause for the impairment of the autophagic-lysosomal pathway (ALP) in many forms of heart disease including cardiac proteinopathy and may play an important pathogenic role; however, the molecular basis and the correcting strategy for the cardiac ALP insufficiency require further investigation. The present study was sought to determine whether myocardial expression and activity of TFEB, the recently identified ALP master regulator, are impaired in a cardiac proteinopathy mouse model and to determine the effect of genetic manipulation of TFEB expression on autophagy and proteotoxicity in a cardiomyocyte model of proteinopathy...
October 7, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28987875/activation-of-igf-1-receptors-and-akt-signaling-by-systemic-hyperinsulinemia-contributes-to-cardiac-hypertrophy-but-does-not-regulate-cardiac-autophagy-in-obese-diabetic-mice
#5
Karla Maria Pires, Marcio Buffolo, Christin Schaaf, J David Symons, James Cox, E Dale Abel, Craig H Selzman, Sihem Boudina
Autophagy plays an important role in the maintenance of normal heart function. However, the role of autophagy in the inulin resistant and diabetic heart is not well understood. Furthermore, the upstream signaling and the downstream targets involved in cardiac autophagy regulation during obesity and type 2 diabetes mellitus (T2DM) are not fully elucidated. The aim of this study was to measure autophagic flux and to dissect the upstream and downstream signaling involved in cardiac autophagy regulation in the hearts of obese T2DM mice...
October 5, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28970090/agxt2-an-unnegligible-aminotransferase-in-cardiovascular-and-urinary-systems
#6
REVIEW
Xiao-Lei Hu, Mu-Peng Li, Pei-Yuan Song, Jie Tang, Xiao-Ping Chen
Cardiovascular diseases (CVDs) and renal impairment interact in a complex and interdependent manner, which makes clarification of possible pathogenesis between CVDs and renal diseases very challenging and important. There is increasing evidence showing that both asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) play a crucial role in the development of CVDs as well as in the prediction of cardiovascular events. Also, the plasma levels of ADMA and SDMA were reported to be significantly associated with renal function...
September 29, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28962857/mitochondrial-cardiomyopathies-feature-increased-uptake-and-diminished-efflux-of-mitochondrial-calcium
#7
Salah Sommakia, Patrick R Houlihan, Sadiki S Deane, Judith A Simcox, Natalia S Torres, Mi-Young Jeong, Dennis R Winge, Claudio J Villanueva, Dipayan Chaudhuri
Calcium (Ca(2+)) influx into the mitochondrial matrix stimulates ATP synthesis. Here, we investigate whether mitochondrial Ca(2+) transport pathways are altered in the setting of deficient mitochondrial energy synthesis, as increased matrix Ca(2+) may provide a stimulatory boost. We focused on mitochondrial cardiomyopathies, which feature such dysfunction of oxidative phosphorylation. We study a mouse model where the main transcription factor for mitochondrial DNA (transcription factor A, mitochondrial, Tfam) has been disrupted selectively in cardiomyocytes...
September 28, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28941705/severe-dcm-phenotype-of-patient-harboring-rbm20-mutation-s635a-can-be-modeled-by-patient-specific-induced-pluripotent-stem-cell-derived-cardiomyocytes
#8
Katrin Streckfuss-Bömeke, Malte Tiburcy, Andrey Fomin, Xiaojing Luo, Wener Li, Claudia Fischer, Cemil Özcelik, Andreas Perrot, Samuel Sossalla, Jan Haas, Ramon Oliveira Vidal, Sabine Rebs, Sara Khadjeh, Benjamin Meder, Stefan Bonn, Wolfgang A Linke, Wolfram-Hubertus Zimmermann, Gerd Hasenfuss, Kaomei Guan
The ability to generate patient-specific induced pluripotent stem cells (iPSCs) provides a unique opportunity for modeling heart disease in vitro. In this study, we generated iPSCs from a patient with dilated cardiomyopathy (DCM) caused by a missense mutation S635A in RNA-binding motif protein 20 (RBM20) and investigated the functionality and cell biology of cardiomyocytes (CMs) derived from patient-specific iPSCs (RBM20-iPSCs). The RBM20-iPSC-CMs showed abnormal distribution of sarcomeric α-actinin and defective calcium handling compared to control-iPSC-CMs, suggesting disorganized myofilament structure and altered calcium machinery in CMs of the RBM20 patient...
September 21, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28923351/functionally-redundant-control-of-cardiac-hypertrophic-signaling-by-inositol-1-4-5-trisphosphate-receptors
#9
M Iveth Garcia, Anja Karlstaedt, Jessica J Chen, Javier Amione-Guerra, Keith A Youker, Heinrich Taegtmeyer, Darren Boehning
Calcium plays an integral role to many cellular processes including contraction, energy metabolism, gene expression, and cell death. The inositol 1, 4, 5-trisphosphate receptor (IP3R) is a calcium channel expressed in cardiac tissue. There are three IP3R isoforms encoded by separate genes. In the heart, the IP3R-2 isoform is reported to being most predominant with regards to expression levels and functional significance. The functional roles of IP3R-1 and IP3R-3 in the heart are essentially unexplored despite measureable expression levels...
September 18, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28923350/ascorbate-starvation-alters-endoplasmic-reticulum-resident-enzymes-in-cardiac-fibroblasts-priming-them-for-increased-procollagen-secretion
#10
Randy T Cowling, Joong Il Park, Ayodeji E Sotimehin, Barry H Greenberg
Since ascorbate is unnecessary for cell growth and survival, cardiac fibroblasts are routinely cultured without it. However, ascorbate is necessary for optimal collagen synthesis, so we hypothesized that its presence would influence cell phenotype. Cardiac fibroblasts cultured without ascorbate had increased intracellular levels of procollagens, with procollagen α1(III) showing the largest accumulation. Endoplasmic reticulum (ER)-resident proteins that are known to bind single-stranded procollagens were also elevated...
September 18, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28919327/endothelial-microparticle-promoted-inhibition-of-vascular-remodeling-is-abrogated-under-hyperglycaemic-conditions
#11
Felix Jansen, Andreas Zietzer, Tobias Stumpf, Anna Flender, Theresa Schmitz, Georg Nickenig, Nikos Werner
BACKGROUND: Endothelial microparticles (EMPs) inhibit vascular remodeling by transferring functional microRNA (miRNA) into target vascular smooth muscle cells (VSMCs). Because EMPs are increased in diabetic patients and potentially linked to vascular complications in diabetes mellitus, we sought to determine whether effects of EMPs generated under high glucose concentration on vascular remodeling might differ from EMPs derived from untreated cells. METHODS AND RESULTS: EMPs were generated from human coronary endothelial cells (HCAEC) exposed to high glucose concentrations in order to mimic diabetic conditions...
September 14, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28886967/class-i-hdacs-control-a-jip1-dependent-pathway-for-kinesin-microtubule-binding-in-cardiomyocytes
#12
Weston W Blakeslee, Ying-Hsi Lin, Matthew S Stratton, Philip D Tatman, Tianjing Hu, Bradley S Ferguson, Timothy A McKinsey
Class I histone deacetylase (HDAC) inhibitors block hypertrophy and fibrosis of the heart by suppressing pathological signaling and gene expression programs in cardiac myocytes and fibroblasts. The impact of HDAC inhibition in unstressed cardiac cells remains poorly understood. Here, we demonstrate that treatment of cultured cardiomyocytes with small molecule HDAC inhibitors leads to dramatic induction of c-Jun amino-terminal kinase (JNK)-interacting protein-1 (JIP1) mRNA and protein expression. In contrast to prior findings, elevated levels of endogenous JIP1 in cardiomyocytes failed to significantly alter JNK signaling or cardiomyocyte hypertrophy...
September 5, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28882480/short-term-administration-of-nicotinamide-mononucleotide-preserves-cardiac-mitochondrial-homeostasis-and-prevents-heart-failure
#13
Rongli Zhang, Yuyan Shen, Lin Zhou, Panjamaporn Sangwung, Hisashi Fujioka, Lilei Zhang, Xudong Liao
Heart failure is associated with mitochondrial dysfunction so that restoring or improving mitochondrial health is of therapeutic importance. Recently, reduction in NAD(+) levels and NAD(+)-mediated deacetylase activity has been recognized as negative regulators of mitochondrial function. Using a cardiac specific KLF4 deficient mouse line that is sensitive to stress, we found mitochondrial protein hyperacetylation coupled with reduced Sirt3 and NAD(+) levels in the heart before stress, suggesting that the KLF4-deficient heart is predisposed to NAD(+)-associated defects...
September 5, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28870504/the-oxidized-phospholipid-povpc-impairs-endothelial-function-and-vasodilation-via-uncoupling-endothelial-nitric-oxide-synthase
#14
Feng-Xia Yan, Hua-Ming Li, Shang-Xuan Li, Shi-Hui He, Wei-Ping Dai, Yan Li, Tian-Tian Wang, Mao-Mao Shi, Hao-Xiang Yuan, Zhe Xu, Jia-Guo Zhou, Da-Sheng Ning, Zhi-Wei Mo, Zhi-Jun Ou, Jing-Song Ou
Endothelial dysfunction is an early stage of atherosclerosis. We recently have shown that 25-hydroxycholesterol found in atherosclerotic lesions could impair endothelial function and vasodilation by uncoupling and inhibiting endothelial nitric oxide synthase (eNOS). 1-Palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC), the oxidation product of oxidized low-density lipoprotein, is another proinflammatory lipid and has also been found in atherosclerotic lesions. However, whether POVPC promotes atherosclerosis like 25-hydroxycholesterol remains unclear...
September 1, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28867536/nitric-oxide-and-camkii-critical-steps-in-the-cardiac-contractile-response-to-igf-1-and-swim-training
#15
Juan I Burgos, Alejandra M Yeves, Jorge P Barrena, Enrique L Portiansky, Martín G Vila-Petroff, Irene L Ennis
Cardiac adaptation to endurance training includes improved contractility by a non-yet clarified mechanism. Since IGF-1 is the main mediator of the physiological response to exercise, we explored its effect on cardiac contractility and the putative involvement of nitric oxide (NO) and CaMKII in control and swim-trained mice. IGF-1 increased cardiomyocyte shortening (128.1±4.6% vs. basal; p˂0.05) and accelerated relaxation (time to 50% relengthening: 49.2±2.0% vs. basal; p˂0.05), effects abrogated by inhibition of: AKT with MK-2206, NO production with the NO synthase (NOS) inhibitor L-NAME and the specific NOS1 inhibitor nitroguanidine (NG), and CaMKII with KN-93...
September 1, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28865712/microrna-31-promotes-adverse-cardiac-remodeling-and-dysfunction-in-ischemic-heart-disease
#16
Eliana C Martinez, Shera Lilyanna, Peipei Wang, Leah A Vardy, Xiaofei Jiang, Arunmozhiarasi Armugam, Kandiah Jeyaseelan, Arthur Mark Richards
RATIONALE: Myocardial infarction (MI) triggers a dynamic microRNA response with the potential of yielding therapeutic targets. OBJECTIVE: We aimed to identify novel aberrantly expressed cardiac microRNAs post-MI with potential roles in adverse remodeling in a rat model, and to provide post-ischemic therapeutic inhibition of a candidate pathological microRNA in vivo. METHODS AND RESULTS: Following microRNA array profiling in rat hearts 2 and 14days post-MI, we identified a time-dependent up-regulation of miR-31 compared to sham-operated rats...
September 1, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28859848/chronic-in-vivo-nitric-oxide-deficiency-impairs-cardiac-functional-recovery-after-ischemia-in-female-but-not-male-mice
#17
Laura A Bienvenu, James Morgan, Melissa E Reichelt, Lea M D Delbridge, Morag J Young
Nitric oxide (NO) is an important regulator of cardiac function and plays a key role in ischemic cardioprotection. The role of chronic NO deficiency in coordinating ischemic vulnerability in female myocardium has not been established. The aim of this study was to determine the influence of chronic in vivo NO synthase inhibition in modulating ex vivo ischemia-reperfusion responses in female hearts (relative to males). Mice were subjected to l-NAME (l-N(G)-Nitroarginine-methyl-ester) treatment in vivo for 8weeks...
August 30, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28843344/novel-common-variants-associated-with-body-mass-index-and-coronary-artery-disease-detected-using-a-pleiotropic-cfdr-method
#18
Wan-Qiang Lv, Xue Zhang, Qiang Zhang, Jing-Yang He, Hui-Min Liu, Xin Xia, Kun Fan, Qi Zhao, Xue-Zhong Shi, Wei-Dong Zhang, Chang-Qing Sun, Hong-Wen Deng
Genome-wide association studies (GWAS) have been successfully applied in identifying single nucleotide polymorphisms (SNPs) associated with body mass index (BMI) and coronary heart disease (CAD). However, the SNPs to date can only explain a small percentage of the genetic variances of traits. Here, we applied a genetic pleiotropic conditional false discovery rate (cFDR) method that combines summary statistic p values from different multi-center GWAS datasets, to detect common genetic variants associated with these two traits...
August 24, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28842242/letter-in-response-to-the-role-of-succinate-and-ros-in-reperfusion-injury-a-critical-appraisal-by-andrienko-et-al
#19
LETTER
David García-Dorado, Antonio Rodríguez-Sinovas, Ignasi Barba, Marisol Ruiz-Meana
No abstract text is available yet for this article.
August 24, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28823816/neonatal-rat-cardiomyocytes-as-an-in-vitro-model-for-circadian-rhythms-in-the-heart
#20
Bastiaan C du Pré, Pieterjan Dierickx, Sandra Crnko, Pieter A Doevendans, Marc A Vos, Niels Geijsen, Didi Neutel, Toon A B van Veen, Linda W van Laake
Circadian rhythms are biorhythms with a 24-hour period that are regulated by molecular clocks. Several clinical and animal models have been developed to analyze the role of these rhythms in cardiovascular physiology, disease and therapy, but a convenient in vitro model that mimics both molecular and functional circadian effects of the heart is not available. Therefore, we established a neonatal rat cardiomyocyte model that recapitulates in vivo circadian rhythmicity, as measured by anti-phasic oscillatory mRNA expression of two core clock genes, Bmal1 and Per2 and that shows functional dependence on the clock as indicated by an oscillating response in apoptosis induced by doxorubicin, hydroperoxide or hypoxia...
August 18, 2017: Journal of Molecular and Cellular Cardiology
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