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Cardiac myocyte

Ayako Uchinaka, Maho Yoshida, Kiyoka Tanaka, Yoshinosuke Hamada, Seiji Mori, Yoshitaka Maeno, Shigeru Miyagawa, Yoshiki Sawa, Kohzo Nagata, Hirofumi Yamamoto, Naomasa Kawaguchi
OBJECTIVE: Left ventricular (LV) remodeling alters the contractile and relaxation properties and induces myocardial stiffness. As LV remodeling progresses, the amount of collagen type III (Col3) is gradually decreased, being replaced by collagen type I (Col1). We evaluated whether Col3 overexpression improved cardiac function and remodeling in a rat with ischemic cardiomyopathy (ICM). We also investigated the functional motif and mechanism of thrombin-cleaved N-terminal osteopontin (N-OPN) on cardiac remodeling...
February 21, 2018: Journal of Thoracic and Cardiovascular Surgery
Muhammad Naveed, Lei Han, Ghulam Jilany Khan, Sufia Yasmeen, Reyaj Mikrani, Muhammad Abbas, Li Cunyu, Zhou Xiaohui
Congestive heart failure (CHF) is a complicated pathophysiological syndrome, leading cause of hospitalization as well as mortalities in developed countries wherein an irregular function of the heart leads to the insufficient blood supply to the body organs. It is an accumulative slackening of various complications including myocardial infarction (MI), coronary heart disease (CAD), hypertension, valvular heart disease (VHD) and cardiomyopathy; its hallmarks include hypertrophy, increased interstitial fibrosis and loss of myocytes...
March 14, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Jaana Rysä, Heikki Tokola, Heikki Ruskoaho
Mechanical forces are able to activate hypertrophic growth of cardiomyocytes in the overloaded myocardium. However, the transcriptional profiles triggered by mechanical stretch in cardiac myocytes are not fully understood. Here, we performed the first genome-wide time series study of gene expression changes in stretched cultured neonatal rat ventricular myocytes (NRVM)s, resulting in 205, 579, 737, 621, and 1542 differentially expressed (>2-fold, P < 0.05) genes in response to 1, 4, 12, 24, and 48 hours of cyclic mechanical stretch...
March 16, 2018: Scientific Reports
Taishi Nakamura, Guangshuo Zhu, Mark J Ranek, Kristen Kokkonen-Simon, Manling Zhang, Grace E Kim, Kenichi Tsujita, David A Kass
BACKGROUND: Stimulation of sGC (soluble guanylate cyclase) or inhibition of PDE5 (phosphodiesterase type 5) activates PKG (protein kinase G)-1α to counteract cardiac hypertrophy and failure. PKG1α acts within localized intracellular domains; however, its oxidation at cysteine 42, linking homomonomers, alters this localization, impairing suppression of pathological cardiac stress. Because PDE5 and sGC reside in separate microdomains, we speculated that PKG1α oxidation might also differentially influence the effects from their pharmacological modulation...
March 2018: Circulation. Heart Failure
Kexin Wang, Yang Xu, Qiong Sun, Jiangang Long, Jiankang Liu, Jian Ding
The multipurpose organelle mitochondria play an essential role(s) in controlling cardiac muscle contraction. Mitochondria, not only function as the powerhouses and the energy source of myocytes, but also modulate intracellular Ca2+ homeostasis, the production of intermediary metabolites/reactive oxygen species (ROS), and other cellular processes. Those molecular events can substantially influence myocardial contraction. Mitochondrial dysfunction is usually associated with cardiac remodeling, and is the causal factor of heart contraction defects in many cases...
March 16, 2018: Free Radical Research
Robert D Johnson, Patrizia Camelliti
The heart is a complex organ composed of multiple cell types, including cardiomyocytes and different non-myocyte populations, all working closely together to determine the hearts properties and maintain normal cardiac function. Connexins are abundantly expressed proteins that form plasma membrane hemichannels and gap junctions between cells. Gap junctions are intracellular channels that allow for communication between cells, and in the heart they play a crucial role in cardiac conduction by coupling adjacent cardiomyocytes...
March 15, 2018: International Journal of Molecular Sciences
Uma Mahesh R Avula, Jonathan J Hernandez, Masatoshi Yamazaki, Carmen R Valdivia, Antony Chu, Alvaro Rojas-Pena, Kuljeet Kaur, Roberto Ramos-Mondragón, Justus M Anumonwo, Stanley Nattel, Héctor H Valdivia, Jérôme Kalifa
BACKGROUND: The mechanisms underlying spontaneous atrial fibrillation (AF) associated with atrial ischemia/infarction are incompletely elucidated. Here, we investigate the mechanisms underlying spontaneous AF in an ovine model of left atrial myocardial infarction (LAMI). METHODS AND RESULTS: LAMI was created by ligating the atrial branch of the left anterior descending coronary artery. ECG loop recorders were implanted to monitor AF episodes. In 7 sheep, dantrolene-a ryanodine receptor blocker-was administered in vivo during the 8-day observation period (LAMI-D, 2...
March 2018: Circulation. Arrhythmia and Electrophysiology
Lorenzo Vannozzi, Immihan Ceren Yasa, Hakan Ceylan, Arianna Menciassi, Leonardo Ricotti, Metin Sitti
Programming materials with tunable physical and chemical interactions among its components pave the way of generating 3D functional active microsystems with various potential applications in tissue engineering, drug delivery, and soft robotics. Here, the development of a recapitulated fascicle-like implantable muscle construct by programmed self-folding of poly(ethylene glycol) diacrylate hydrogels is reported. The system comprises two stacked layers, each with differential swelling degrees, stiffnesses, and thicknesses in 2D, which folds into a 3D tube together...
March 14, 2018: Macromolecular Bioscience
Jerry C Madukwe, Elisabeth E Garland-Kuntz, Angeline M Lyon, Alan V Smrcka
Phospholipase C (PLC) enzymes hydrolyze membrane phosphatidylinositol 4,5 bisphosphate (PIP2) and regulate Ca2+ and protein kinase signaling in virtually all mammalian cell types. Chronic activation of the PLCɛ isoform downstream of G protein-coupled receptors (GPCRs) contributes to the development of cardiac hypertrophy. We have previously shown that PLCε-catalyzed hydrolysis of Golgi-associated phosphatidylinositol 4-phosphate (PI4P) in cardiac myocytes depends on G protein βγ subunits released upon stimulation with endothelin-1...
March 13, 2018: Journal of Biological Chemistry
Wen Dun, Peter Danilo, Peter J Mohler, Penelope A Boyden
Cardiac Na+ channel remodeling provides a critical substrate for generation of reentrant arrhythmias in border zones of the infarcted canine heart. Recent studies show that Nav1.5 cytoskeletal- and endosomal-based membrane trafficking and function are linked to tubulin, microtubular (MT) networks, and Eps15 homology domain containing proteins like EHD4. AIM: Our objective is to understand the relation of tubulin and EHD4 to Nav 1.5 channel protein remodeling observed in border zone cells (IZs) when arrhythmias are known to occur; that is, 3-h, 48-h and 5-day post coronary occlusion...
March 10, 2018: Life Sciences
Katharina Schleicher, Manuela Zaccolo
3',5'-cyclic adenosine monophosphate (cAMP) signalling plays a major role in the cardiac myocyte response to extracellular stimulation by hormones and neurotransmitters. In recent years, evidence has accumulated demonstrating that the cAMP response to different extracellular agonists is not uniform: depending on the stimulus, cAMP signals of different amplitudes and kinetics are generated in different subcellular compartments, eliciting defined physiological effects. In this review, we focus on how real-time imaging using fluorescence resonance energy transfer (FRET)-based reporters has provided mechanistic insight into the compartmentalisation of the cAMP signalling pathway and allowed for the precise definition of the regulation and function of subcellular cAMP nanodomains...
March 13, 2018: Journal of Cardiovascular Development and Disease
Jonathan James Weldrick, Mohammad Abdul-Ghani, Lynn A Megeney, Patrick G Burgon
The capacity to isolate and study single cardiomyocytes has dramatically enhanced our understanding of the fundamental mechanisms of the heart. Currently, two primary methods for the isolation of cardiomyocytes are employed; i) The neonatal isolation protocol and, ii) the Langendorff isolation method. A major limiting feature of both procedures is the inability to isolate cardiomyocytes between 3 days and 3 weeks post-birth. Herein we report the establishment and validation of a new method for the rapid and efficient isolation of mouse cardiomyocytes, regardless of age...
March 13, 2018: Canadian Journal of Physiology and Pharmacology
Sha Yan, Pengfei Huang, Ying Wang, Xiongzhi Zeng, Yiya Zhang
Spider venoms are known to contain various toxins that are used as an effective means to capture their prey or to defend themselves against predators. An investigation of the properties of Ornithoctonus huwena (O.huwena) crude venom found that the venom can block neuromuscular transmission of isolated mouse phrenic nerve-diaphragm and sciatic nerve-sartorius preparations. However, little is known about its electrophysiological effects on cardiac myocytes. In this study, electrophysiological activities of ventricular myocytes were detected by 100 μg/mL venom of O...
March 13, 2018: Channels
Bence Hegyi, Julie Bossuyt, Leigh G Griffiths, Rafael Shimkunas, Zana Coulibaly, Zhong Jian, Kristin N Grimsrud, Claus S Sondergaard, Kenneth S Ginsburg, Nipavan Chiamvimonvat, Luiz Belardinelli, András Varró, Julius G Papp, Piero Pollesello, Jouko Levijoki, Leighton T Izu, W Douglas Boyd, Tamás Bányász, Donald M Bers, Ye Chen-Izu
Heart failure (HF) following myocardial infarction (MI) is associated with high incidence of cardiac arrhythmias. Development of therapeutic strategy requires detailed understanding of electrophysiological remodeling. However, changes of ionic currents in ischemic HF remain incompletely understood, especially in translational large-animal models. Here, we systematically measure the major ionic currents in ventricular myocytes from the infarct border and remote zones in a porcine model of post-MI HF. We recorded eight ionic currents during the cell's action potential (AP) under physiologically relevant conditions usingself AP-clamp sequential dissection...
March 12, 2018: Proceedings of the National Academy of Sciences of the United States of America
Valentina Prando, Francesca Da Broi, Mauro Franzoso, Anna Pia Plazzo, Nicola Pianca, Maura Francolini, Cristina Basso, Matthew W Kay, Tania Zaglia, Marco Mongillo
AIM: Cardiac sympathetic neurons (SNs) finely tune the rate and strength of heart contractions to match the blood demand, both at rest and during acute stresses, through the release of norepinephrine (NE). Junctional sites at the interface between the two cell types have been observed, but whether direct neuro-cardiac coupling has a role in heart physiology has not thus far been clearly demonstrated. METHODS AND RESULTS: We investigated the dynamics of SN/cardiomyocyte intercellular signalling, both by FRET-based imaging of cAMP in co-cultures, as a readout of cardiac β-AR activation, and in vivo, using optogenetics in transgenic mice with SN-specific expression of Channelrhodopsin-2...
March 10, 2018: Journal of Physiology
Kimberly L Dodge-Kafka, Moriah Gildart, Jinliang Li, Hrishikesh Thakur, Michael S Kapiloff
Class IIa histone deacetylases (HDACs) are transcriptional repressors whose nuclear export in the cardiac myocyte is associated with the induction of pathological gene expression and cardiac remodeling. Class IIa HDACs are regulated by multiple, functionally opposing post-translational modifications, including phosphorylation by protein kinase D (PKD) that promotes nuclear export and phosphorylation by protein kinase A (PKA) that promotes nuclear import. We have previously shown that the scaffold protein muscle A-kinase anchoring protein β (mAKAPβ) orchestrates signaling in the cardiac myocyte required for pathological cardiac remodeling, including serving as a scaffold for both PKD and PKA...
March 6, 2018: Journal of Molecular and Cellular Cardiology
Timothy D Bryson, Xiaosong Gu, Remonda M Khalil, Safa Khan, Liping Zhu, Jiang Xu, Edward Peterson, Xiao-Ping Yang, Pamela Harding
BACKGROUND: Prostaglandin E2 (PGE2 ) signals through 4 separate G-protein coupled receptor sub-types to elicit a variety of physiologic and pathophysiological effects. We recently reported that PGE2 via its EP3 receptor could reduce cardiac contractility of isolated myocytes and the working heart preparation. We thus hypothesized that there is an imbalance in the EP3/EP4 ratio towards EP3 in the failing heart and that overexpression of EP4 in a mouse model of heart failure would improve cardiac function...
March 6, 2018: Journal of Molecular and Cellular Cardiology
Ni Yang, Liuzhong Wu, Ying Zhao, Ning Zou, Chunfeng Liu
It is generally accepted that insulin exerts an antiapoptotic effect against ischemia/reperfusion through the activation of PI3K/Akt/mTOR pathway. MicroRNAs involve in multiple cardiac pathophysiological processes, including ischemia/reperfusion-induced cardiac injury. However, the regulation of microRNAs in the cardioprotective effect of insulin is rarely discussed. In this study, using a cell model of ischemia through culturing H9C2 cardiac myocytes in serum-free medium with hypoxia, we demonstrated that pretreatment with insulin significantly inhibited cell apoptosis and downregulated microRNA-320 (miR-320) expression...
March 9, 2018: Cell Biochemistry and Function
Sebastian Polak, Klaus Romero, Alexander Berg, Nikunjkumar Patel, Masoud Jamei, David Hermann, Debra Hanna
Cardiotoxicity is among the top drug safety concerns, and is of specific interest in tuberculosis, where this is a known or potential adverse event of current and emerging treatment regimens. As there is a need for a tool, beyond the QT interval, to quantify cardiotoxicity early in drug development, an empirical decision tree based classifier was developed to predict the risk of Torsades de pointes (TdP). The cardiac risk algorithm was developed using pseudo-electrocardiogram (ECG) outputs derived from cardiac myocyte electromechanical model simulations of increasing concentrations of 96 reference compounds which represented a range of clinical TdP risk...
March 8, 2018: Journal of Pharmacokinetics and Pharmacodynamics
David Charles Hutchings, Simon George Anderson, Jessica L Caldwell, Andrew W Trafford
Novel cardioprotective agents are needed in both heart failure (HF) and myocardial infarction. Increasing evidence from cellular studies and animal models indicate protective effects of phosphodiesterase-5 (PDE5) inhibitors, drugs usually reserved as treatments of erectile dysfunction and pulmonary arterial hypertension. PDE5 inhibitors have been shown to improve contractile function in systolic HF, regress left ventricular hypertrophy, reduce myocardial infarct size and suppress ischaemia-induced ventricular arrhythmias...
March 8, 2018: Heart: Official Journal of the British Cardiac Society
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