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Cardiac myocyte

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https://www.readbyqxmd.com/read/29150591/cholesterol-depletion-does-not-alter-the-capacitance-or-ca-handling-of-the-surface-or-t-tubule-membranes-in-mouse-ventricular-myocytes
#1
Hanne C Gadeberg, Cherrie H T Kong, Simon M Bryant, Andrew F James, Clive H Orchard
Cholesterol is a key component of the cell plasma membrane. It has been suggested that the t-tubule membrane of cardiac ventricular myocytes is enriched in cholesterol and that this plays a role in determining t-tubule structure and function. We have used methyl-β-cyclodextrin (MβCD) to deplete cholesterol in intact and detubulated mouse ventricular myocytes to investigate the contribution of cholesterol to t-tubule structure, membrane capacitance, and the distribution of Ca flux pathways. Depletion of membrane cholesterol was confirmed using filipin; however, di-8-ANEPPS staining showed no differences in t-tubule structure following MβCD treatment...
November 2017: Physiological Reports
https://www.readbyqxmd.com/read/29150444/toll-like-receptor-4-induced-ryanodine-receptor-2-oxidation-and-sarcoplasmic-reticulum-ca2-leakage-promote-cardiac-contractile-dysfunction-in-sepsis
#2
Jie Yang, Rui Zhang, Xin Jiang, Jingzhang Lv, Ying Li, Hongyu Ye, Wenjuan Liu, Gang Wang, Cuicui Zhang, Na Zheng, Ming Dong, Yan Wang, Peiya Chen, Kumar Santosh, Yong Jiang, Jie Liu
Studies suggest the potential role of sarcoplasmic reticulum (SR) Ca2+ leak in cardiac contractile dysfunction in sepsis. However, direct supporting evidence is lacking, and the mechanisms underlying this SR leak are poorly understood. Here, we investigated the changes in cardiac Ca2+ handling and contraction in LPS-treated rat cardiomyocytes and a mouse model of polymicrobial sepsis produced by cecal ligation and puncture (CLP). LPS decreased the systolic Ca2+ transient and myocyte contraction, as well as SR Ca2+ content...
November 17, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29145393/estimating-the-probabilities-of-rare-arrhythmic-events-in-multiscale-computational-models-of-cardiac-cells-and-tissue
#3
Mark A Walker, Viatcheslav Gurev, John J Rice, Joseph L Greenstein, Raimond L Winslow
Ectopic heartbeats can trigger reentrant arrhythmias, leading to ventricular fibrillation and sudden cardiac death. Such events have been attributed to perturbed Ca2+ handling in cardiac myocytes leading to spontaneous Ca2+ release and delayed afterdepolarizations (DADs). However, the ways in which perturbation of specific molecular mechanisms alters the probability of ectopic beats is not understood. We present a multiscale model of cardiac tissue incorporating a biophysically detailed three-dimensional model of the ventricular myocyte...
November 2017: PLoS Computational Biology
https://www.readbyqxmd.com/read/29141899/atypical-g-protein-%C3%AE-5-promotes-cardiac-oxidative-stress-apoptosis-and-fibrotic-remodeling-in-response-to-multiple-cancer-chemotherapeutics
#4
Biswanath Maity, Sreemoyee Chakraborti, Arnab Pramanick, Sudipta Saha, Somnath Singha Roy, Arnab Ray Chaudhuri, Madhusudan Das, Sujoy Ghosh, Adele Stewart
The clinical use of multiple classes of cancer chemotherapeutics is limited by irreversible, dose-dependent, and sometimes life-threatening cardiotoxicity. We report here that, though distinct in their mechanisms of action, doxorubicin, paclitaxel, and 5-FU all induce rapid and robust upregulation of atypical G protein Gβ5 in the myocardium, correlating with oxidative stress, myocyte apoptosis, and the accumulation of pro-inflammatory and pro-fibrotic cytokines. In ventricular cardiac myocytes (VCM), Gβ5 deficiency provided substantial protection against the cytotoxic actions of chemotherapeutics, including reductions in oxidative stress and simultaneous attenuation of ROS-dependent activation of the ATM and CaMKII pro-apoptotic signaling cascades...
November 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/29141748/trypanosoma-cruzi-infection-induces-pannexin-1-channel-opening-in-cardiac-myocytes
#5
Iván Barría, Juan Güiza, Fredi Cifuentes, Pedro Zamorano, Juan C Sáez, Jorge González, José L Vega
Trypanosoma cruzi, the etiological agent of Chagas diseases, invades the cardiac tissue causing acute myocarditis and heart electrical disturbances. In T. cruzi invasion, the parasite induces [Ca(2+)]i transients in the host cells, an essential phenomenon for invasion. To date, knowledge on the mechanism that elicits transients of [Ca(2+)]i during the infection of cardiac myocytes has not been fully characterized. Pannexin1 (Panx1) channel are poorly selective channels found in all vertebrates that serve as a pathway for ATP release...
November 6, 2017: American Journal of Tropical Medicine and Hygiene
https://www.readbyqxmd.com/read/29137484/the-role-of-endogenous-reactive-oxygen-species-in-cardiac-myocyte-autophagy
#6
J-P Wang, R-F Chi, J Liu, Y-Z Deng, X-B Han, F-Z Qin, B Li
Autophagy is implicated in the maintenance of cardiac homeostasis. Autophagy is activated in heart failure, in which reactive oxygen species (ROS) are increased. Exogenous ROS have been shown to induce cardiomyocyte autophagy alterations. However, little is known about the influences of physiological levels of endogenous ROS on cardiomyocyte autophagy. In the present study, we tested the hypothesis that endogenous ROS in cardiomyocytes play an important role in inducing autophagy. Cultured H9C2 cardiomyocytes or Sprague-Dawley rats were treated with the antioxidant N-acetyl-cysteine (NAC) or the superoxide dismutase mimic tempol under the basal or nutrient deprivation conditions...
November 10, 2017: Physiological Research
https://www.readbyqxmd.com/read/29136124/what-is-the-clinical-significance-of-ventricular-mural-antagonism
#7
Paul P Lunkenheimer, Peter Niederer, Robert S Stephenson, Klaus Redmann, Randas V Batista, Morten Smerup, Robert H Anderson
Recent morphological studies provide evidence that the ventricular walls are arranged as a 3D meshwork of aggregated cardiomyocyte chains, exhibiting marked local structural variations. In contrary to previous findings, up to two-fifths of the chains are found to have a partially transmural alignment, thus deviating from the prevailing tangential orientation. Upon contraction, they produce, in addition to a tangential force, a radial force component that counteracts ventricular constriction and aids widening of the ventricular cavity...
November 9, 2017: European Journal of Cardio-thoracic Surgery
https://www.readbyqxmd.com/read/29135437/an-adaptation-of-astronomical-image-processing-enables-characterization-and-functional-3d-mapping-of-individual-sites-of-excitation-contraction-coupling-in-rat-cardiac-muscle
#8
Qinghai Tian, Lars Kaestner, Laura Schröder, Jia Guo, Peter Lipp
In beating cardiomyocytes, synchronized localized Ca(2+) transients from thousands of active excitation-contraction coupling sites (ECC couplons) comprising plasma and sarcoplasmic reticulum membrane calcium channels are important determinants of the heart's performance. Nevertheless, our knowledge about their properties is limited by the lack of appropriate experimental and analysis strategies. We designed CaCLEAN to untangle fundamental characteristics of ECC couplons by combining the astronomer's CLEAN algorithm with known properties of calcium diffusion...
November 14, 2017: ELife
https://www.readbyqxmd.com/read/29131758/titin-gene-and-protein-functions-in-passive-and-active-muscle
#9
Wolfgang A Linke
The thin and thick filaments of muscle sarcomeres are interconnected by the giant protein titin, which is a scaffolding filament, signaling platform, and provider of passive tension and elasticity in myocytes. This review summarizes recent insight into the mechanisms behind how titin gene mutations cause hereditary cardiomyopathy and how titin protein is mechanically active in skeletal and cardiac myocytes. A main theme is the evolving role of titin as a modulator of contraction. Topics include strain-sensing via titin in the sarcomeric A-band as the basis for length-dependent activation, titin elastic recoil and refolding of titin domains as an energy source, and Ca(2+)-dependent stiffening of titin stretched during eccentric muscle contractions...
November 13, 2017: Annual Review of Physiology
https://www.readbyqxmd.com/read/29129702/fkbp8-protects-the-heart-from-hemodynamic-stress-by-preventing-the-accumulation-of-misfolded-proteins-and-endoplasmic-reticulum-associated-apoptosis-in-mice
#10
Tomofumi Misaka, Tomokazu Murakawa, Kazuhiko Nishida, Yosuke Omori, Manabu Taneike, Shigemiki Omiya, Chris Molenaar, Yoshihiro Uno, Osamu Yamaguchi, Junji Takeda, Ajay M Shah, Kinya Otsu
Protein quality control in cardiomyocytes is crucial to maintain cellular homeostasis. The accumulation of damaged organelles, such as mitochondria and misfolded proteins in the heart is associated with heart failure. During the process to identify novel mitochondria-specific autophagy (mitophagy) receptors, we found FK506-binding protein 8 (FKBP8), also known as FKBP38, shares similar structural characteristics with a yeast mitophagy receptor, autophagy-related 32 protein. However, knockdown of FKBP8 had no effect on mitophagy in HEK293 cells or H9c2 myocytes...
November 9, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29128504/biophysical-comparison-of-sodium-currents-in-native-cardiac-myocytes-and-human-induced-pluripotent-stem-cell-derived-cardiomyocytes
#11
Robert J Goodrow, Suveer Desai, Jacqueline A Treat, Brian K Panama, Mayurika Desai, Vladislav V Nesterenko, Jonathan M Cordeiro
INTRODUCTION: Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are used for safety pharmacology and to investigate genetic diseases affecting cardiac ion channels. It is unclear whether adult myocytes or hiPSC-CMs are the better platform for cardiac safety pharmacology. We examined the biophysical and molecular properties of INa in adult myocytes and hiPSC-CMs. METHODS: hiPSC-CMs were plated at low density. Atrial and ventricular cells were obtained from dog hearts...
November 8, 2017: Journal of Pharmacological and Toxicological Methods
https://www.readbyqxmd.com/read/29127073/estrogen-receptor-beta-maintains-expression-of-klf15-to-prevent-cardiac-myocyte-hypertrophy-in-female-rodents
#12
Neil Hoa, Lisheng Ge, Kenneth S Korach, Ellis R Levin
Maintaining a healthy, anti-hypertrophic state in the heart prevents progression to cardiac failure. In humans, angiotensin II (AngII) indirectly and directly stimulates hypertrophy and progression, while estrogens acting through estrogen receptor beta (ERβ) inhibit these AngII actions. The KLF15 transcription factor has been purported to provide anti-hypertrophic action. In cultured neonatal rat cardiomyocytes, we found AngII inhibited KLF1 expression and nuclear localization, substantially prevented by estradiol (E2) or β-LGND2 (β-LGND2), an ERβ agonist...
November 7, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/29126879/mechanical-stretch-increases-l-type-calcium-channel-stability-in-cardiomyocytes-through-a-polycystin-1-akt-dependent-mechanism
#13
A Córdova-Casanova, I Olmedo, J A Riquelme, G Barrientos, G Sánchez, T G Gillette, S Lavandero, M Chiong, P Donoso, Z Pedrozo
The L-type calcium channel (LTCC) is an important determinant of cardiac contractility. Therefore, changes in LTCC activity or protein levels could be expected to affect cardiac function. Several studies describing LTCC regulation are available, but only a few examine LTCC protein stability. Polycystin-1 (PC1) is a mechanosensor that regulates heart contractility and is involved in mechanical stretch-induced cardiac hypertrophy. PC1 was originally described as an unconventional Gi/o protein-coupled receptor in renal cells...
November 7, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29124057/radiation-induced-cardiovascular-disease-a-clinical-perspective
#14
REVIEW
Syed Wamique Yusuf, Bhanu Prasad Venkatesulu, Lakshmi Shree Mahadevan, Sunil Krishnan
Cancer survival has improved dramatically, and this has led to the manifestation of late side effects of multimodality therapy. Radiation (RT) to the thoracic malignancies results in unintentional irradiation of the cardiac chambers. RT-induced microvascular ischemia leads to disruption of capillary endothelial framework, and injury to differentiated myocytes results in deposition of collagen and fibrosis. Coexistence of risk factors of metabolic syndrome and preexisting atherosclerosis in addition to RT exposure results in accelerated occurrence of major coronary events...
2017: Frontiers in Cardiovascular Medicine
https://www.readbyqxmd.com/read/29123976/advanced-glycation-end-products-reduce-the-calcium-transient-in-cardiomyocytes-by-increasing-production-of-reactive-oxygen-species-and-nitric-oxide
#15
Zeinab Hegab, Tamer M A Mohamed, Nicholas Stafford, Mamas Mamas, Elizabeth J Cartwright, Delvac Oceandy
Advanced glycation end products (AGE) are central to the development of cardiovascular complications associated with diabetes mellitus. AGE may alter cellular function through cross-linking of cellular proteins or by activating the AGE receptor (RAGE). However, the signalling molecules involved during AGE stimulation in cardiomyocytes remain unclear. Here, we investigated the effects of AGE treatment on intracellular calcium homeostasis of isolated cardiomyocytes and studied the activation of signalling molecules involved in this process...
November 2017: FEBS Open Bio
https://www.readbyqxmd.com/read/29123207/atropine-augments-cardiac-contractility-by-inhibiting-camp-specific-phosphodiesterase-type-4
#16
Ruwan K Perera, Thomas H Fischer, Michael Wagner, Matthias Dewenter, Christiane Vettel, Nadja I Bork, Lars S Maier, Marco Conti, Juergen Wess, Ali El-Armouche, Gerd Hasenfuß, Viacheslav O Nikolaev
Atropine is a clinically relevant anticholinergic drug, which blocks inhibitory effects of the parasympathetic neurotransmitter acetylcholine on heart rate leading to tachycardia. However, many cardiac effects of atropine cannot be adequately explained solely by its antagonism at muscarinic receptors. In isolated mouse ventricular cardiomyocytes expressing a Förster resonance energy transfer (FRET)-based cAMP biosensor, we confirmed that atropine inhibited acetylcholine-induced decreases in cAMP. Unexpectedly, even in the absence of acetylcholine, after G-protein inactivation with pertussis toxin or in myocytes from M2- or M1/3-muscarinic receptor knockout mice, atropine increased cAMP levels that were pre-elevated with the β-adrenergic agonist isoproterenol...
November 9, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29121733/pheochromocytoma-as-a-reversible-cause-of-cardiomyopathy-analysis-and-review-of-the-literature
#17
Rong Zhang, Deepashree Gupta, Stewart G Albert
CONTEXT: Pheochromocytoma and paraganglioma are rare neuroendocrine tumors which overproduce catecholamines and arise from the adrenal gland or extra-adrenal chromaffin cells of the sympathetic and parasympathetic ganglia (1). Excessive catecholamine-induced stimulation of cardiac myocytes leads to damage which manifests in several forms ranging from Takotsubo to dilated cardiomyopathy. Diagnosis of pheochromocytoma-related cardiomyopathies is often delayed due to the atypical presentation associated with many cases...
December 15, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/29117535/rescuing-infusion-of-mirna-1-prevents-cardiac-remodeling-in-a-heart-selective-mirna-deficient-mouse
#18
Shuilian Luo, Yuhang Chen, Rui He, Yujun Shi, Li Su
OBJECTIVE: The decreased expression of muscle-specific microRNA-1 (miR-1) has been found in many cardiovascular diseases and is considered to contribute to heart failure (HF). Here we investigated the role of miR-1 in myocardium protection by infusion of miR-1 in a cardiac global miRNA-deficient mouse. METHODS: We generated a cardiac-selective miRNA-deficient mouse by crossing Dicer(flox/flox) mice with mice expressing tamoxifen-inducible Cre recombinase under the control of a mouse αMHC promoter...
November 5, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29117223/sensitivity-analysis-revealing-the-effect-of-modulating-ionic-mechanisms-on-calcium-dynamics-in-simulated-human-heart-failure
#19
Maria T Mora, Jose M Ferrero, Lucia Romero, Beatriz Trenor
Abnormal intracellular Ca2+ handling is the major contributor to the depressed cardiac contractility observed in heart failure. The electrophysiological remodeling associated with this pathology alters both the action potential and the Ca2+ dynamics, leading to a defective excitation-contraction coupling that ends in mechanical dysfunction. The importance of maintaining a correct intracellular Ca2+ concentration requires a better understanding of its regulation by ionic mechanisms. To study the electrical activity and ionic homeostasis of failing myocytes, a modified version of the O'Hara et al...
2017: PloS One
https://www.readbyqxmd.com/read/29116876/preservation-of-functional-microvascular-bed-is-vital-for-long-term-survival-of-cardiac-myocytes-within-large-transmural-post-myocardial-infarction-scar
#20
Colleen Nofi, Yevgen Bogatyryov, Eduard I Dedkov
This study was aimed to understand the mechanism of persistent cardiac myocyte (CM) survival in myocardial infarction (MI) scars. A transmural MI was induced in 12-month-old Sprague-Dawley rats by permanent coronary artery ligation. The hearts were collected 3 days, 1, 2, 4, 8, and 12 weeks after MI and evaluated with histology, immunohistochemistry, and quantitative morphometry. Vasculature patency was assessed in 4-, 8-, and 12-week-old scars by infusion of 15-micron microspheres into the left ventricle before euthanasia...
November 1, 2017: Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society
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