Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
The hollow, muscular organ that maintains the circulation of the blood.
The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation.
The volume of BLOOD passing through the HEART per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with STROKE VOLUME (volume per beat).
Contractile activity of the MYOCARDIUM.
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.
Enlargement of the HEART, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both HEART VENTRICLES or HEART ATRIA. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of CARDIOMYOPATHIES.
Surgery performed on the heart.
Mature contractile cells, commonly known as myocytes, that form one of three kinds of muscle. The three types of muscle cells are skeletal (MUSCLE FIBERS, SKELETAL), cardiac (MYOCYTES, CARDIAC), and smooth (MYOCYTES, SMOOTH MUSCLE). They are derived from embryonic (precursor) muscle cells called MYOBLASTS.
Unexpected rapid natural death due to cardiovascular collapse within one hour of initial symptoms. It is usually caused by the worsening of existing heart diseases. The sudden onset of symptoms, such as CHEST PAIN and CARDIAC ARRHYTHMIAS, particularly VENTRICULAR TACHYCARDIA, can lead to the loss of consciousness and cardiac arrest followed by biological death. (from Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed., 2005)
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
The hemodynamic and electrophysiological action of the HEART VENTRICLES.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Long-lasting voltage-gated CALCIUM CHANNELS found in both excitable and nonexcitable tissue. They are responsible for normal myocardial and vascular smooth muscle contractility. Five subunits (alpha-1, alpha-2, beta, gamma, and delta) make up the L-type channel. The alpha-1 subunit is the binding site for calcium-based antagonists. Dihydropyridine-based calcium antagonists are used as markers for these binding sites.
Regulation of the rate of contraction of the heart muscles by an artificial pacemaker.
The chambers of the heart, to which the BLOOD returns from the circulation.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
An electrophysiologic technique for studying cells, cell membranes, and occasionally isolated organelles. All patch-clamp methods rely on a very high-resistance seal between a micropipette and a membrane; the seal is usually attained by gentle suction. The four most common variants include on-cell patch, inside-out patch, outside-out patch, and whole-cell clamp. Patch-clamp methods are commonly used to voltage clamp, that is control the voltage across the membrane and measure current flow, but current-clamp methods, in which the current is controlled and the voltage is measured, are also used.
An electrogenic ion exchange protein that maintains a steady level of calcium by removing an amount of calcium equal to that which enters the cells. It is widely distributed in most excitable membranes, including the brain and heart.
Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
Pathological conditions involving the HEART including its structural and functional abnormalities.
Compression of the heart by accumulated fluid (PERICARDIAL EFFUSION) or blood (HEMOPERICARDIUM) in the PERICARDIUM surrounding the heart. The affected cardiac functions and CARDIAC OUTPUT can range from minimal to total hemodynamic collapse.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).
Refers to animals in the period of time just after birth.
Elements of limited time intervals, contributing to particular results or situations.
The excitable plasma membrane of a muscle cell. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)
Procedures in which placement of CARDIAC CATHETERS is performed for therapeutic or diagnostic procedures.
Signal transduction mechanisms whereby calcium mobilization (from outside the cell or from intracellular storage pools) to the cytoplasm is triggered by external stimuli. Calcium signals are often seen to propagate as waves, oscillations, spikes, sparks, or puffs. The calcium acts as an intracellular messenger by activating calcium-responsive proteins.
Cell membrane glycoproteins that are selectively permeable to potassium ions. At least eight major groups of K channels exist and they are made up of dozens of different subunits.
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
Myosin type II isoforms found in cardiac muscle.
Cessation of heart beat or MYOCARDIAL CONTRACTION. If it is treated within a few minutes, heart arrest can be reversed in most cases to normal cardiac rhythm and effective circulation.
Drugs that selectively bind to and activate beta-adrenergic receptors.
A network of tubules and sacs in the cytoplasm of SKELETAL MUSCLE FIBERS that assist with muscle contraction and relaxation by releasing and storing calcium ions.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).
Theoretical representations that simulate the behavior or activity of the cardiovascular system, processes, or phenomena; includes the use of mathematical equations, computers and other electronic equipment.
Precursor cells destined to differentiate into cardiac myocytes (MYOCYTES, CARDIAC).
Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
The repeating contractile units of the MYOFIBRIL, delimited by Z bands along its length.
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
A state of subnormal or depressed cardiac output at rest or during stress. It is a characteristic of CARDIOVASCULAR DISEASES, including congenital, valvular, rheumatic, hypertensive, coronary, and cardiomyopathic. The serious form of low cardiac output is characterized by marked reduction in STROKE VOLUME, and systemic vasoconstriction resulting in cold, pale, and sometimes cyanotic extremities.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
Cyclopentanophenanthrenes with a 5- or 6-membered lactone ring attached at the 17-position and SUGARS attached at the 3-position. Plants they come from have long been used in congestive heart failure. They increase the force of cardiac contraction without significantly affecting other parameters, but are very toxic at larger doses. Their mechanism of action usually involves inhibition of the NA(+)-K(+)-EXCHANGING ATPASE and they are often used in cell biological studies for that purpose.
The geometric and structural changes that the HEART VENTRICLES undergo, usually following MYOCARDIAL INFARCTION. It comprises expansion of the infarct and dilatation of the healthy ventricle segments. While most prevalent in the left ventricle, it can also occur in the right ventricle.
One of the three polypeptide chains that make up the TROPONIN complex. It inhibits F-actin-myosin interactions.
The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.
The quantity of volume or surface area of CELLS.
Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic.
Calcium-transporting ATPases that catalyze the active transport of CALCIUM into the SARCOPLASMIC RETICULUM vesicles from the CYTOPLASM. They are primarily found in MUSCLE CELLS and play a role in the relaxation of MUSCLES.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
A tetrameric calcium release channel in the SARCOPLASMIC RETICULUM membrane of SMOOTH MUSCLE CELLS, acting oppositely to SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES. It is important in skeletal and cardiac excitation-contraction coupling and studied by using RYANODINE. Abnormalities are implicated in CARDIAC ARRHYTHMIAS and MUSCULAR DISEASES.
Visualization of the heart structure and cardiac blood flow for diagnostic evaluation or to guide cardiac procedures via techniques including ENDOSCOPY (cardiac endoscopy, sometimes refered to as cardioscopy), RADIONUCLIDE IMAGING; MAGNETIC RESONANCE IMAGING; TOMOGRAPHY; or ULTRASONOGRAPHY.
One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
The hemodynamic and electrophysiological action of the left HEART VENTRICLE. Its measurement is an important aspect of the clinical evaluation of patients with heart disease to determine the effects of the disease on cardiac performance.
The mitochondria of the myocardium.
An impulse-conducting system composed of modified cardiac muscle, having the power of spontaneous rhythmicity and conduction more highly developed than the rest of the heart.
Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue.
A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).
A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes SMOOTH MUSCLE, stimulates CARDIAC MUSCLE, stimulates DIURESIS, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide PHOSPHODIESTERASES, antagonism of ADENOSINE RECEPTORS, and modulation of intracellular calcium handling.
The transference of a heart from one human or animal to another.
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
A form of CARDIAC MUSCLE disease that is characterized by ventricular dilation, VENTRICULAR DYSFUNCTION, and HEART FAILURE. Risk factors include SMOKING; ALCOHOL DRINKING; HYPERTENSION; INFECTION; PREGNANCY; and mutations in the LMNA gene encoding LAMIN TYPE A, a NUCLEAR LAMINA protein.
A conical fibro-serous sac surrounding the HEART and the roots of the great vessels (AORTA; VENAE CAVAE; PULMONARY ARTERY). Pericardium consists of two sacs: the outer fibrous pericardium and the inner serous pericardium. The latter consists of an outer parietal layer facing the fibrous pericardium, and an inner visceral layer (epicardium) resting next to the heart, and a pericardial cavity between these two layers.
A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight PEPTIDES derived from a common precursor and secreted mainly by the HEART ATRIUM. All these peptides share a sequence of about 20 AMINO ACIDS.
Occurrence of heart arrest in an individual when there is no immediate access to medical personnel or equipment.
The study of the electrical activity and characteristics of the HEART; MYOCARDIUM; and CARDIOMYOCYTES.
Ion channels that specifically allow the passage of SODIUM ions. A variety of specific sodium channel subtypes are involved in serving specialized functions such as neuronal signaling, CARDIAC MUSCLE contraction, and KIDNEY function.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
The volume of the HEART, usually relating to the volume of BLOOD contained within it at various periods of the cardiac cycle. The amount of blood ejected from a ventricle at each beat is STROKE VOLUME.
A process fundamental to muscle physiology whereby an electrical stimulus or action potential triggers a myocyte to depolarize and contract. This mechanical muscle contraction response is regulated by entry of calcium ions into the cell.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
The innermost layer of the heart, comprised of endothelial cells.
Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.
The relationship between the dose of an administered drug and the response of the organism to the drug.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
The ability of a substrate to allow the passage of ELECTRONS.
One of the three polypeptide chains that make up the TROPONIN complex. It is a cardiac-specific protein that binds to TROPOMYOSIN. It is released from damaged or injured heart muscle cells (MYOCYTES, CARDIAC). Defects in the gene encoding troponin T result in FAMILIAL HYPERTROPHIC CARDIOMYOPATHY.
Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART.) Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY, collateral flow from other coronary vascular beds, or reversal of vasospasm.
Developmental abnormalities involving structures of the heart. These defects are present at birth but may be discovered later in life.
Examinations used to diagnose and treat heart conditions.
A condition in which the LEFT VENTRICLE of the heart was functionally impaired. This condition usually leads to HEART FAILURE; MYOCARDIAL INFARCTION; and other cardiovascular complications. Diagnosis is made by measuring the diminished ejection fraction and a depressed level of motility of the left ventricular wall.
The heart of the fetus of any viviparous animal. It refers to the heart in the postembryonic period and is differentiated from the embryonic heart (HEART/embryology) only on the basis of time.
The larger subunits of MYOSINS. The heavy chains have a molecular weight of about 230 kDa and each heavy chain is usually associated with a dissimilar pair of MYOSIN LIGHT CHAINS. The heavy chains possess actin-binding and ATPase activity.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.
The amount of BLOOD pumped out of the HEART per beat, not to be confused with cardiac output (volume/time). It is calculated as the difference between the end-diastolic volume and the end-systolic volume.
Enlargement of the LEFT VENTRICLE of the heart. This increase in ventricular mass is attributed to sustained abnormal pressure or volume loads and is a contributor to cardiovascular morbidity and mortality.
Potassium channel whose permeability to ions is extremely sensitive to the transmembrane potential difference. The opening of these channels is induced by the membrane depolarization of the ACTION POTENTIAL.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
The hemodynamic and electrophysiological action of the HEART ATRIA.
Acidic protein found in SARCOPLASMIC RETICULUM that binds calcium to the extent of 700-900 nmoles/mg. It plays the role of sequestering calcium transported to the interior of the intracellular vesicle.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-1 receptors are equally sensitive to EPINEPHRINE and NOREPINEPHRINE and bind the agonist DOBUTAMINE and the antagonist METOPROLOL with high affinity. They are found in the HEART, juxtaglomerular cells, and in the central and peripheral nervous systems.
The opening and closing of ion channels due to a stimulus. The stimulus can be a change in membrane potential (voltage-gated), drugs or chemical transmitters (ligand-gated), or a mechanical deformation. Gating is thought to involve conformational changes of the ion channel which alters selective permeability.
An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
The long cylindrical contractile organelles of STRIATED MUSCLE cells composed of ACTIN FILAMENTS; MYOSIN filaments; and other proteins organized in arrays of repeating units called SARCOMERES .
Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.
The restoration of the sequential order of contraction and relaxation of the HEART ATRIA and HEART VENTRICLES by atrio-biventricular pacing.
Tumors in any part of the heart. They include primary cardiac tumors and metastatic tumors to the heart. Their interference with normal cardiac functions can cause a wide variety of symptoms including HEART FAILURE; CARDIAC ARRHYTHMIAS; or EMBOLISM.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
The artificial substitution of heart and lung action as indicated for HEART ARREST resulting from electric shock, DROWNING, respiratory arrest, or other causes. The two major components of cardiopulmonary resuscitation are artificial ventilation (RESPIRATION, ARTIFICIAL) and closed-chest CARDIAC MASSAGE.
Institutions specializing in the care of patients with heart disorders.
A light microscopic technique in which only a small spot is illuminated and observed at a time. An image is constructed through point-by-point scanning of the field in this manner. Light sources may be conventional or laser, and fluorescence or transmitted observations are possible.
A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)
A GATA transcription factor that is expressed in the MYOCARDIUM of developing heart and has been implicated in the differentiation of CARDIAC MYOCYTES. GATA4 is activated by PHOSPHORYLATION and regulates transcription of cardiac-specific genes.
Isoforms of MYOSIN TYPE II, specifically found in the ventricular muscle of the HEART. Defects in the genes encoding ventricular myosins result in FAMILIAL HYPERTROPHIC CARDIOMYOPATHY.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A group of enzymes that are dependent on CYCLIC AMP and catalyze the phosphorylation of SERINE or THREONINE residues on proteins. Included under this category are two cyclic-AMP-dependent protein kinase subtypes, each of which is defined by its subunit composition.
Conical muscular projections from the walls of the cardiac ventricles, attached to the cusps of the atrioventricular valves by the chordae tendineae.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
The rate dynamics in chemical or physical systems.
Large, multinucleate single cells, either cylindrical or prismatic in shape, that form the basic unit of SKELETAL MUSCLE. They consist of MYOFIBRILS enclosed within and attached to the SARCOLEMMA. They are derived from the fusion of skeletal myoblasts (MYOBLASTS, SKELETAL) into a syncytium, followed by differentiation.
A group of slow opening and closing voltage-gated potassium channels. Because of their delayed activation kinetics they play an important role in controlling ACTION POTENTIAL duration.
Use of electric potential or currents to elicit biological responses.
A methylpyrrole-carboxylate from RYANIA that disrupts the RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL to modify CALCIUM release from SARCOPLASMIC RETICULUM resulting in alteration of MUSCLE CONTRACTION. It was previously used in INSECTICIDES. It is used experimentally in conjunction with THAPSIGARGIN and other inhibitors of CALCIUM ATPASE uptake of calcium into SARCOPLASMIC RETICULUM.
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
Post-systolic relaxation of the HEART, especially the HEART VENTRICLES.
A 43-kDa peptide which is a member of the connexin family of gap junction proteins. Connexin 43 is a product of a gene in the alpha class of connexin genes (the alpha-1 gene). It was first isolated from mammalian heart, but is widespread in the body including the brain.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Proteins to which calcium ions are bound. They can act as transport proteins, regulator proteins, or activator proteins. They typically contain EF HAND MOTIFS.
One of the minor protein components of skeletal muscle. Its function is to serve as the calcium-binding component in the troponin-tropomyosin B-actin-myosin complex by conferring calcium sensitivity to the cross-linked actin and myosin filaments.
General or unspecified injuries to the heart.
An enzyme that catalyzes the active transport system of sodium and potassium ions across the cell wall. Sodium and potassium ions are closely coupled with membrane ATPase which undergoes phosphorylation and dephosphorylation, thereby providing energy for transport of these ions against concentration gradients.
Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic beta-antagonists are used for treatment of hypertension, cardiac arrhythmias, angina pectoris, glaucoma, migraine headaches, and anxiety.
Gated, ion-selective glycoproteins that traverse membranes. The stimulus for ION CHANNEL GATING can be due to a variety of stimuli such as LIGANDS, a TRANSMEMBRANE POTENTIAL DIFFERENCE, mechanical deformation or through INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS.
The movement of ions across energy-transducing cell membranes. Transport can be active, passive or facilitated. Ions may travel by themselves (uniport), or as a group of two or more ions in the same (symport) or opposite (antiport) directions.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
A class of drugs that act by inhibition of potassium efflux through cell membranes. Blockade of potassium channels prolongs the duration of ACTION POTENTIALS. They are used as ANTI-ARRHYTHMIA AGENTS and VASODILATOR AGENTS.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
General increase in bulk of a part or organ due to CELL ENLARGEMENT and accumulation of FLUIDS AND SECRETIONS, not due to tumor formation, nor to an increase in the number of cells (HYPERPLASIA).
A caveolin that is expressed exclusively in MUSCLE CELLS and is sufficient to form CAVEOLAE in SARCOLEMMA. Mutations in caveolin 3 are associated with multiple muscle diseases including DISTAL MYOPATHY and LIMB-GIRDLE MUSCULAR DYSTROPHY.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
A voltage-gated sodium channel subtype that mediates the sodium ion PERMEABILITY of CARDIOMYOCYTES. Defects in the SCN5A gene, which codes for the alpha subunit of this sodium channel, are associated with a variety of CARDIAC DISEASES that result from loss of sodium channel function.
Modified cardiac muscle fibers composing the terminal portion of the heart conduction system.
A condition in which HEART VENTRICLES exhibit impaired function.
A shaker subfamily of potassium channels that participate in transient outward potassium currents by activating at subthreshold MEMBRANE POTENTIALS, inactivating rapidly, and recovering from inactivation quickly.
The pressure within a CARDIAC VENTRICLE. Ventricular pressure waveforms can be measured in the beating heart by catheterization or estimated using imaging techniques (e.g., DOPPLER ECHOCARDIOGRAPHY). The information is useful in evaluating the function of the MYOCARDIUM; CARDIAC VALVES; and PERICARDIUM, particularly with simultaneous measurement of other (e.g., aortic or atrial) pressures.
The veins and arteries of the HEART.
A PEPTIDE that is secreted by the BRAIN and the HEART ATRIA, stored mainly in cardiac ventricular MYOCARDIUM. It can cause NATRIURESIS; DIURESIS; VASODILATION; and inhibits secretion of RENIN and ALDOSTERONE. It improves heart function. It contains 32 AMINO ACIDS.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
Fibers composed of MICROFILAMENT PROTEINS, which are predominately ACTIN. They are the smallest of the cytoskeletal filaments.
Agents that increase calcium influx into calcium channels of excitable tissues. This causes vasoconstriction in VASCULAR SMOOTH MUSCLE and/or CARDIAC MUSCLE cells as well as stimulation of insulin release from pancreatic islets. Therefore, tissue-selective calcium agonists have the potential to combat cardiac failure and endocrinological disorders. They have been used primarily in experimental studies in cell and tissue culture.
A form of CARDIAC MUSCLE disease, characterized by left and/or right ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR; HYPERTROPHY, RIGHT VENTRICULAR), frequent asymmetrical involvement of the HEART SEPTUM, and normal or reduced left ventricular volume. Risk factors include HYPERTENSION; AORTIC STENOSIS; and gene MUTATION; (FAMILIAL HYPERTROPHIC CARDIOMYOPATHY).
An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.
Diversion of the flow of blood from the entrance of the right atrium directly to the aorta (or femoral artery) via an oxygenator thus bypassing both the heart and lungs.
A diverse superfamily of proteins that function as translocating proteins. They share the common characteristics of being able to bind ACTINS and hydrolyze MgATP. Myosins generally consist of heavy chains which are involved in locomotion, and light chains which are involved in regulation. Within the structure of myosin heavy chain are three domains: the head, the neck and the tail. The head region of the heavy chain contains the actin binding domain and MgATPase domain which provides energy for locomotion. The neck region is involved in binding the light-chains. The tail region provides the anchoring point that maintains the position of the heavy chain. The superfamily of myosins is organized into structural classes based upon the type and arrangement of the subunits they contain.
Compounds of four rings containing a nitrogen. They are biosynthesized from reticuline via rearrangement of scoulerine. They are similar to BENZYLISOQUINOLINES. Members include chelerythrine and sanguinarine.
The measurement of an organ in volume, mass, or heaviness.
A delayed rectifier subtype of shaker potassium channels that conducts a delayed rectifier current. It contributes to ACTION POTENTIAL repolarization of MYOCYTES in HEART ATRIA.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
The circulation of blood through the CORONARY VESSELS of the HEART.
A condition that is characterized by episodes of fainting (SYNCOPE) and varying degree of ventricular arrhythmia as indicated by the prolonged QT interval. The inherited forms are caused by mutation of genes encoding cardiac ion channel proteins. The two major forms are ROMANO-WARD SYNDROME and JERVELL-LANGE NIELSEN SYNDROME.
The small mass of modified cardiac muscle fibers located at the junction of the superior vena cava (VENA CAVA, SUPERIOR) and right atrium. Contraction impulses probably start in this node, spread over the atrium (HEART ATRIUM) and are then transmitted by the atrioventricular bundle (BUNDLE OF HIS) to the ventricle (HEART VENTRICLE).
Flaps of tissue that prevent regurgitation of BLOOD from the HEART VENTRICLES to the HEART ATRIA or from the PULMONARY ARTERIES or AORTA to the ventricles.
Period of contraction of the HEART, especially of the HEART VENTRICLES.
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
A subclass of alpha-adrenergic receptors that mediate contraction of SMOOTH MUSCLE in a variety of tissues such as ARTERIOLES; VEINS; and the UTERUS. They are usually found on postsynaptic membranes and signal through GQ-G11 G-PROTEINS.
Agents that emit light after excitation by light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
Cation-transporting proteins that utilize the energy of ATP hydrolysis for the transport of CALCIUM. They differ from CALCIUM CHANNELS which allow calcium to pass through a membrane without the use of energy.
A transferase that catalyzes formation of PHOSPHOCREATINE from ATP + CREATINE. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic ISOENZYMES have been identified in human tissues: the MM type from SKELETAL MUSCLE, the MB type from myocardial tissue and the BB type from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
A potentially lethal cardiac arrhythmia that is characterized by uncoordinated extremely rapid firing of electrical impulses (400-600/min) in HEART VENTRICLES. Such asynchronous ventricular quivering or fibrillation prevents any effective cardiac output and results in unconsciousness (SYNCOPE). It is one of the major electrocardiographic patterns seen with CARDIAC ARREST.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
Methods to induce and measure electrical activities at specific sites in the heart to diagnose and treat problems with the heart's electrical system.
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
A family of non-enveloped viruses infecting mammals (MASTADENOVIRUS) and birds (AVIADENOVIRUS) or both (ATADENOVIRUS). Infections may be asymptomatic or result in a variety of diseases.
A device designed to stimulate, by electric impulses, contraction of the heart muscles. It may be temporary (external) or permanent (internal or internal-external).
Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.
Abnormal fluid retention by the body due to impaired cardiac function or heart failure. It is usually characterized by increase in venous and capillary pressure, and swollen legs when standing. It is different from the generalized edema caused by renal dysfunction (NEPHROTIC SYNDROME).
One of the three polypeptide chains that make up the TROPONIN complex of skeletal muscle. It is a calcium-binding protein.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
A cardioactive glycoside consisting of rhamnose and ouabagenin, obtained from the seeds of Strophanthus gratus and other plants of the Apocynaceae; used like DIGITALIS. It is commonly used in cell biological studies as an inhibitor of the NA(+)-K(+)-EXCHANGING ATPASE.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
Compounds which inhibit or antagonize the biosynthesis or actions of phosphodiesterases.
One of the POTASSIUM CHANNEL BLOCKERS, with secondary effect on calcium currents, which is used mainly as a research tool and to characterize channel subtypes.
In screening and diagnostic tests, the probability that a person with a positive test is a true positive (i.e., has the disease), is referred to as the predictive value of a positive test; whereas, the predictive value of a negative test is the probability that the person with a negative test does not have the disease. Predictive value is related to the sensitivity and specificity of the test.
Drugs that selectively bind to and activate alpha adrenergic receptors.
A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.
Carrier of aroma of butter, vinegar, coffee, and other foods.
A multifunctional calcium-calmodulin-dependent protein kinase subtype that occurs as an oligomeric protein comprised of twelve subunits. It differs from other enzyme subtypes in that it lacks a phosphorylatable activation domain that can respond to CALCIUM-CALMODULIN-DEPENDENT PROTEIN KINASE KINASE.
An abnormally rapid ventricular rhythm usually in excess of 150 beats per minute. It is generated within the ventricle below the BUNDLE OF HIS, either as autonomic impulse formation or reentrant impulse conduction. Depending on the etiology, onset of ventricular tachycardia can be paroxysmal (sudden) or nonparoxysmal, its wide QRS complexes can be uniform or polymorphic, and the ventricular beating may be independent of the atrial beating (AV dissociation).
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
Treatment process involving the injection of fluid into an organ or tissue.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

Morphine mimics preconditioning via free radical signals and mitochondrial K(ATP) channels in myocytes. (1/8946)

BACKGROUND: We tried to determine whether morphine mimics preconditioning (PC) to reduce cell death in cultured cardiomyocytes and whether opioid delta(1) receptors, free radicals, and K(ATP) channels mediate this effect. METHODS AND RESULTS: Chick embryonic ventricular myocytes were studied in a flow-through chamber while flow rate, pH, and O(2) and CO(2) tension were controlled. Cardiomyocyte viability was quantified with propidium iodide (5 micromol/L), and production of free radicals was measured with 2',7'-dichlorofluorescin diacetate. PC with 10 minutes of simulated ischemia before 10 minutes of reoxygenation or morphine (1 micromol/L) or BW373U86 (10 pmol/L) infusion for 10 minutes followed by a 10-minute drug-free period before 1 hour of ischemia and 3 hours of reoxygenation reduced cell death to the same extent (*P:<0.05) (PC, 20+/-1%, n=7*; morphine, 32+/-4%, n=8*; BW373U86, 21+/-6%; controls, 52+/-5%, n=8). Like PC, morphine and BW373U86 increased free radical production 2-fold before ischemia (0.35+/-0.10, n=6*; 0.41+/-0.08, n=4* versus controls, 0.15+/-0.05, n=8, arbitrary units). Protection and increased free radical signals during morphine infusion were abolished with either the thiol reductant 2-mercaptopropionyl glycine (400 micromol/L), an antioxidant; naloxone (10 micromol/L), a nonselective morphine receptor antagonist; BNTX (0.1 micromol/L), a selective opioid delta(1) receptor antagonist; or 5-hydroxydecanoate (100 micromol/L), a selective mitochondrial K(ATP) channel antagonist. CONCLUSIONS: These results suggest that direct stimulation of cardiocyte opioid delta(1) receptors leads to activation of mitochondrial K(ATP) channels. The resultant increase of intracellular free radical signals may be an important component of the signaling pathways by which morphine mimics preconditioning in cardiomyocytes.  (+info)

Treatment with a growth hormone secretagogue in a model of developing heart failure: effects on ventricular and myocyte function. (2/8946)

BACKGROUND: Exogenous administration of growth hormone (GH) and subsequently increased production of insulin-like growth factor-1 can influence left ventricular (LV) myocardial growth and geometry in the setting of congestive heart failure (CHF). This study determined the effects of an orally active GH secretagogue (GHS) treatment that causes a release of endogenous GH on LV function and myocyte contractility in a model of developing CHF. METHODS AND RESULTS: Pigs were randomly assigned to the following treatment groups: (1) chronic rapid pacing at 240 bpm for 3 weeks (n=11); (2) chronic rapid pacing and GHS (CP-424,391 at 10 mg x kg(-1) x d(-1), n=9); and (3) sham controls (n=8). In the untreated pacing CHF group, LV fractional shortening was reduced (21+/-2% versus 47+/-2%) and peak wall stress increased (364+/-21 versus 141+/-5 g/cm(2)) from normal control values (P:<0.05). In the GHS group, LV fractional shortening was higher (29+/-2%) and LV peak wall stress lower (187+/-126 g/cm(2)) than untreated CHF values (P:<0.05). With GHS treatment, the ratio of LV mass to body weight increased by 44% from untreated values. Steady-state myocyte velocity of shortening was reduced with pacing CHF compared with controls (38+/-1 versus 78+/-1 microm/s, P:<0.05) and was increased from pacing CHF values with GHS treatment (55+/-7 microm/s, P:<0.05). CONCLUSIONS: The improved LV pump function that occurred with GHS treatment in this model of CHF was most likely a result of favorable effects on LV myocardial remodeling and contractile processes. On the basis of these results, further studies are warranted to determine the potential role of GH secretagogues in the treatment of CHF.  (+info)

Eicosanoids participate in the regulation of cardiac glucose transport by contribution to a rearrangement of actin cytoskeletal elements. (3/8946)

Intact actin microfilaments are required for insulin-regulated glucose transporter isoform 4 (GLUT4) translocation to the plasma membrane. Lipoxygenase (LO) metabolites have recently been shown to contribute to the regulation of actin cytoskeleton rearrangement. In the present investigation, ventricular cardiomyocytes were used to study the effects of two structurally different LO inhibitors (esculetin and nordihydroguaiaretic acid) on insulin signalling events, glucose uptake, GLUT4 translocation and the actin network organization. Insulin stimulation increased glucose uptake 3-fold in control cells, whereas LO inhibition completely blocked this effect. This was paralleled by a slight reduction in the insulin-induced tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and IRS-2. However, inhibition of 12-LO did not affect the association of phosphatidylinositol 3-kinase with IRS-1 and the phosphorylation of Akt/protein kinase B in response to insulin. Addition of 12(S)-hydroxyeicosatetraenoic acid almost completely restored the insulin action in cells exposed to nordihydroguaiaretic acid. Insulin stimulation increased cell surface GLUT4 2-fold in control cells, whereas LO inhibition abrogated the insulin-stimulated GLUT4 translocation. LO inhibition induced a prominent disassembly of actin fibres compared with control cells. In conclusion, we show here that 12(S)-hydroxyeicosatetraenoic acid plays a role in the organization of the actin network in cardiomyocytes. LO inhibition blocks GLUT4 translocation without affecting downstream insulin signalling. These data suggest that LO metabolites participate in the regulation of glucose transport by contributing to a rearrangement of actin cytoskeletal elements.  (+info)

Stimulation by melittin of Na+-Ca2+ exchange current in ventricular myocytes of guinea pigs. (4/8946)

AIM: To study the mechanism of calcium overload induced by melittin in myocytes. METHODS: Whole cell patch-clamp technique was applied for recording the currents. RESULTS: Mel 0.05, 0.1 micromol/L increased the peak amplitude of I(Na) (nA) from -2.1+/-0.8 to -3.2+/-1.0 (n=7, P < 0.05) and -3.7+/-1.5 (n=7, P < 0.05) respectively at testing potential of -40 mV. Mel 0.05, 0.1, 0.2 micromol/L had no significant effect on I(Ca), but enhanced I(Na-Ca) (pA) from 53+/-21 to 427+/-256 (n=5, P < 0.05), 349+/-147 (n=5, P<0.01) and 320+/-97 (n=5, P < 0.05) respectively at a testing potential of +50 mV. CONCLUSION: The stimulating effect of Mel on I(Na-Ca) rather than the effect on I(Ca) contributes to the calcium overload of myocytes.  (+info)

Inhibitory effects of berberine on IK1, IK, and HERG channels of cardiac myocytes. (5/8946)

AIM: To study the effects of berberine on inward rectifier potassium current (IK1) and outward delayed rectifier potassium current (IK) of guinea pig ventricular myocytes, and on human ether-a-go-go related gene (HERG) channel expressed in Xenopus oocytes. METHODS: Whole cell patch-clamp and geneclamp techniques were used to record ionic currents. RESULTS: Berberine prolonged action potential duration (APD) and inhibited IK1 and IK in a concentration-dependent manner. Berberine 100 micromol/L increased APD90 from (450 +\- 48) ms to (888 +\- 90) ms (n = 6, P < 0.01), and inhibited IK1 by 65 % +\- 7 % (n = 6, P < 0.01). Berberine 50 micromol/L inhibited IK by 57 % +\- 6 %, IKtail by 53 % +\- 6 % (n = 6, P < 0.01). Berberine produced a voltage-dependent block on IK that increased with stronger depolarization, and once all channels were activated, there was no further block at positive potentials. Berberine blocked the HERG channels potently with an IC50 value of approximately 75 micromol/L. This block was voltage-dependent, suggesting that it probably bind to either open or inactivated HERG channels. CONCLUSION: Berberine prolonged APD and possessed blocking effect on IK1, IK, and HERG channel expressed in Xenopus oocytes. The antiarrhythmic mechanism of berberine is related to its inhibitory effects on IK1, IK, and HERG channel.  (+info)

Effects of matrine, artemisinin, tetrandrine on cytosolic [Ca2+]i in guinea pig ventricular myocytes. (6/8946)

AIM: To compare the effects of matrine, artemisinin, and tetrandrine on intracellular Ca2+ concentration ([Ca2+]i) in guinea pig ventricular myocytes. METHODS: A single ventricular myocyte was loaded with Fluo 3-acetoxymethyl (Fluo 3-AM). [Ca2+]i was recorded by laser scanning confocal microscope and represented by fluorescence intensity (FI). RESULTS: 1) KCl 60 mmol . L-1 elevated the FI from 299 +/ -19 to 1389 +/- 325 (P < 0.01) in the presence of extracellular Ca2+ 1.8 mmol . L-1. 2) Both matrine and artemisinin at the concentration of 100 micromol . L-1 could enhance the increase of FI by KCl 60 mmol . L-1. The FI values reached 1495 +/- 320 and 1646 +/- 308 from 301 +/- 14 and 299 +/- 16 (P < 0.01), respectively. 3) Both tetrandrine 1, 10, and 100 micromol . L-1 and verapamil 10 micromol . L-1 inhibited the influx of extracellular Ca2+ induced by KCl 60 mmol . L-1. 4) Matrine 1, 10, and 100 micromol . L-1 could elevate the FI in the presence of extracellular Ca2+. The FI values reached 441 +/- 96, 504 +/- 112, and 643 +/- 126 from 303 +/- 27, 300 +/- 32, and 296 +/- 19 (P < 0.05), respectively. 5) Tetrandrine 1 and 10 micromol . L-1 could apparently inhibited Ca2+ release from intracellular calcium stores induced by caffeine 20 mmol . L-1 (P < 0.05). CONCLUSION: Effects of matrine, artemisinin, and tetrandrine on [Ca2+ )]i in ventricular  (+info)

Inhibitory effect of quercetin on cultured neonatal rat cardiomyocytes hypertrophy induced by angiotensin. (7/8946)

AIM: To study the inhibitory effect of quercetin on cultured neonatal rat cardiomyocytes hypertrophy induced by angiotensin II (AngII) and its mechanism. METHODS: DNA, RNA, and protein synthesis were measured by incorporation of [3H]thymidine, [14C]uridine, and [3H]tyrosine, respectively. Protein content were measured by Lowry's method. Protein kinase C (PKC) activity was assayed by incubating PKC with histone IIIS and [gamma-(32)P]ATP. Tyrosine protein kinase (TPK) activity was assayed by incubating TPK with poly glutamate/tyrosine (4:1) and [gamma-(32P]ATP. RESULTS: After treated with AngIIat 10 nmol/L for 24 h, total protein content was greatly increased as compared with untreated group (P < 0.01). Incorporation of [14C]uridine and [3H]tyrosine was also greatly increased (P < 0.01) respectively, while incorporation of [3H]thymidine remained unchanged (P > 0.05). Ang II strongly increased cardiomyocytes PKC and TPK activities at 30 min. Que (1-100 micromol/L) could inhibit the increase of total protein content, incorporation of [14C]uridine and [3H]tyrosine, and PKC and TPK activities induced by Ang II in concentration-dependent manner. CONCLUSION: The inhibitory effect of Que on the cardiomyocytes hypertrophy was related to its inhibitory effect on PKC and TPK.  (+info)

Effect of sea anemone toxin anthopleurin-Q on sodium current in guinea pig ventricular myocytes. (8/8946)

AIM: To investigate the effects of a sea anemone toxin anthopleurin-Q (AP-Q) isolated from Anthopleura xanthogrammica on sodium current (INa) in isolated guinea pig ventricular myocytes. METHODS: Single myocytes were dissociated by enzymatic dissociation method. INa was recorded using whole-cell patch-clamp technique. RESULTS: AP-Q (3 - 300 nmol/L) increased INa in a concentration-dependent manner. The EC50 value for increasing INa was 104 nmol/L (95 % confidence range: 78 - 130 nmol/L). AP-Q 300 nmol/L shifted the I-V curve to the leftward, changed the membrane potential of half maximal activation to more negative potential from (-36.3 +/- 2.3) mV to (-43 +/- 3) mV (n = 6, P < 0.01) and changed the membrane potential of half maximal inactivation to more positive potential from (-75 +/- 6) mV to (-59 +/- 5) mV (n = 6, P < 0.01). AP-Q 300 nmol/L shortened the half-recovery time of INa from (114 +/- 36) ms to (17 +/- 2) ms (n = 6, P < 0.01). The fast inactivation time constant (tauf) of INa was markedly increased by AP-Q 300 nmol/L. CONCLUSION: AP-Q has a stimulating effect on I(Na) with slowing the inactivation course of INa.  (+info)

Human Cardiomyocytes Stem Cell Culture Extra-cellular Differentiation Matrix is essential for Differentiation of Human Cardiomyocytes Stem Cell Cultures. This product requires Human Cardiomyocytes Stem Cell Culture Media Cat#M36003-04 and Cells Cat# 36003-04. Also available Products ...
TY - JOUR. T1 - Mechanochemotransduction during cardiomyocyte contraction is mediated by localized nitric oxide signaling. AU - Jian, Zhong. AU - Han, Huilan. AU - Zhang, Tieqiao. AU - Puglisi, Jose. AU - Izu, Leighton T. AU - Shaw, John A.. AU - Onofiok, Ekama. AU - Erickson, Jeffery R.. AU - Chen, Yi-Je. AU - Horvath, Balazs. AU - Shimkunas, Rafael. AU - Xiao, Wenwu. AU - Li, Yuanpei. AU - Pan, Tingrui. AU - Chan, James W. AU - Banyasz, Tamas. AU - Tardiff, Jil C.. AU - Chiamvimonvat, Nipavan. AU - Bers, Donald M. AU - Lam, Kit. AU - Chen-Izu, Ye. PY - 2014/3/18. Y1 - 2014/3/18. N2 - Cardiomyocytes contract against a mechanical load during each heartbeat, and excessive mechanical stress leads to heart diseases. Using a cell-in-gel system that imposes an afterload during cardiomyocyte contraction, we found that nitric oxide synthase (NOS) was involved in transducing mechanical load to alter Ca2+ dynamics. In mouse ventricular myocytes, afterload increased the systolic Ca2+ transient, which ...
The thioredoxin interaction protein (TXNIP) has been reported to be closely related to cell oxidative stress, apoptosis and inflammation. TXNIP is involved in the regulation of oxidative stress in lung and renal injury. However, it is unclear as to whether it participates in the protective effects of sevoflurane preconditioning in cardiomyocyte injury caused by oxidative stress in ischemia. In the present study, H9c2 cardiomyocytes were cultured with 0, 1.5, 2, 3.5, 5 or 6% sevoflurane for 3 h, followed by exposure to oxygen and glucose deprivation. The results demonstrated that oxygen and glucose deprivation induced an increase in TXNIP expression, lactate dehydrogenase (LDH) release, caspase‑3 activity, reactive oxygen species and malondialdehyde production. Preconditioning of the H9c2 cells with 3.5% sevoflurane suppressed TXNIP expression, LDH leakage, caspase‑3 activity, reactive oxygen species and malondialdehyde production, and it promoted cell viability. TXNIP overexpression reversed ...
Full Text - Inducing cardiomyocyte proliferation is a hopeful approach for cardiac regeneration following myocardial infarction. Previous studies have shown that p21 inhibits the cardiomyocyte proliferation and cardiac regeneration. Deacetylation of p21 by Sirt1 deacetylase may reduce p21 abundance and remove p21-induced cell cycle arrest. However, whether p21 deacetylation and Sirt1 deacetylate control cardiomyocyte proliferation is unclear. Here, we show that acetylation of p21 induces cardiomyocyte proliferation arrest, whereas blocking the acetylation of p21 increases cardiomyocyte proliferation. P21 can be acetylated by Sirt1, and Sirt1 activate p21 ubiquitination through deacetylation. Additionally, overexpression of Sirt1 induces EdU-, pH3-, and Aurora B-positive cardiomyocytes in neonatal and adult mice. In contrast, depletion of Sirt1 reduces cardiomyocyte proliferation in vitro and in vivo. Moreover, Sirt1 protects cardiac function, reduces cardiac remodeling, inhibits
The apelin peptide is described as one of the most potent inotropic agents, produced endogenously in a wide range of cells, including cardiomyocytes. Despite positive effects on cardiac contractility in multicellular preparations, as well as indications of cardio-protective actions in several diseases, its effects and mechanisms of action at the cellular level are incompletely understood. Here, we report apelin effects on dynamic mechanical characteristics of single ventricular cardiomyocytes, isolated from mouse models (control, apelin-deficient [Apelin-KO], apelin-receptor KO mouse [APJ-KO]), and rat. Dynamic changes in maximal velocity of cell shortening and relaxation were monitored. In addition, more traditional indicators of inotropic effects, such as maximum shortening (in mechanically unloaded cells) or peak force development (in auxotonic contracting cells, preloaded using the carbon fibre technique) were studied. The key finding is that, using Apelin-KO cardiomyocytes exposed to different
In vitro human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs) can differentiate into functional cardiomyocytes (CMs). Protocols for cardiac differentiation of hESCs and
Intracellular calcium (Ca) cycling plays a central role in cardiac excitation-contraction coupling.1,2 Ca alternans, a beat-to-beat alternation in intracellular Ca transient amplitude, is an important factor promoting T-wave alternans and pulsus alternans, markers conferring an increased risk of sudden cardiac death.3 Although Ca alternans has been widely studied in cardiac myocytes,4-13 the underlying mechanism remains controversial. Eisner et al4 were the first to propose that Ca alternans could be explained by a steep nonlinear dependence of sarcoplasmic reticulum (SR) Ca release on the diastolic SR Ca load immediately preceding the release (a steep fractional release-load relationship). This mechanism requires that diastolic SR Ca load alternate concomitantly with SR Ca release. Subsequent experimental6,7,9 and theoretical9,14,15 studies have provided evidence supporting this mechanism. However, later experimental studies in rabbit ventricular myocytes by Picht et al12 and in cat atrial ...
A new impedimetric detection of cardiotoxicity induced by doxorubicin in cultured neonatal rat cardiomyocytes, Lin Wei, Shao-Feng Wang, Hong-Wei Gu, Xia Li
The present study demonstrates that (1) human PF has a greater trophic effect than human serum on cultured rat adult cardiac myocytes, which is likely due to a high concentration of FGF2, and (2) both serum and PF from patients with cardiac hypertrophy have additional effects on cardiac myocytes that are related to the increase in LV mass and that suggest the presence of a circulating growth factor(s) involved in the process of hypertrophy.. One of the major findings of the present study is that PF has a hypertrophic effect on cardiac myocytes, as indicated by (1) the increase of MyHC mRNA level, (2) increased rate of protein synthesis, and (3) increase in total protein content. This trophic effect is not associated with a shift in myosin isoforms, since both α- and β-MyHC mRNAs increase. Furthermore, PF does not seem to enhance apoptosis, since the percentage of cells dying in culture was the same under all experimental conditions (Table 1⇑).. The greater trophic effect of PF on cardiac ...
Detection of cardiomyocyte death is crucial for the diagnosis and treatment of heart disease. Here we use comparative methylome analysis to identify genomic loci that are unmethylated specifically in cardiomyocytes, and develop these as biomarkers to quantify cardiomyocyte DNA in circulating cell-free DNA (cfDNA) derived from dying cells. Plasma of healthy individuals contains essentially no cardiomyocyte cfDNA, consistent with minimal cardiac turnover. Patients with acute ST-elevation myocardial infarction show a robust cardiac cfDNA signal that correlates with levels of troponin and creatine phosphokinase (CPK), including the expected elevation-decay dynamics following coronary angioplasty. Patients with sepsis have high cardiac cfDNA concentrations that strongly predict mortality, suggesting a major role of cardiomyocyte death in mortality from sepsis. A cfDNA biomarker for cardiomyocyte death may find utility in diagnosis and monitoring of cardiac pathologies and in the study of normal human cardiac
The second messenger cyclic adenosine monophosphate (cAMP) is the most important modulator of sympathetic control over cardiac contractility. In cardiac myocytes and many other cell types, however, cAMP transduces the signal generated upon stimulation of various receptors and activates different cellular functions, raising the issue of how specificity can be achieved. In the general field of signal transduction, the view is emerging that specificity is guaranteed by tight localization of signaling events. Here, we show that in neonatal rat cardiac myocytes, beta-adrenergic stimulation generates multiple microdomains with increased concentration of cAMP in correspondence with the region of the transverse tubule/junctional sarcoplasmic reticulum membrane. The restricted pools of cAMP show a range of action as small as approximately 1 micrometer, and free diffusion of the second messenger is limited by the activity of phosphodiesterases. Furthermore, we demonstrate that such gradients of cAMP specifically
Transverse tubules (T-tubules) are orderly invaginations of the sarcolemma in mammalian cardiomyocytes. The integrity of T-tubule architecture is critical for cardiac excitation-contraction coupling function. T-tubule remodeling is recognized as a key player in cardiac dysfunction. Early studies on T-tubule structure were based on electron microscopy, which uncovered important information about the T-tubule architecture. The advent of fluorescent membrane probes allowed the application of confocal microscopy to investigations of T-tubule structure. Studies have now been extended beyond single cardiomyocytes to examine the T-tubule network in intact hearts through in situ confocal imaging of Langendorff-perfused hearts. This technique has allowed visualization of T-tubule organization in their natural habitat, avoiding the damage induced by isolation of cardiomyocytes. Additionally, it is possible to obtain T-tubule images in different subepicardial regions in a single intact heart. We review how this
The regenerative potential of the adult heart is very limited and insufficient to replace damaged muscle mass in the diseased heart. Recent advances in cardiac cell therapy and tissue engineering fuel new hope for the development of novel therapeutic approaches with the aim to trigger myocardial regeneration after injury. Stem cell-derived cardiomyocytes represent ideal candidates for cardiac cell-based therapeutic strategies, and current research focuses on the development of cardiac constructs for implantation. Despite the cardiogenic properties of the newly generated cardiomyocytes, these cells present a heterogeneous and immature phenotype, which is more comparable with cardiomyocytes of early developmental stages. However, successful employment of these new cardiomyocytes for myocardial repair demands that the physiological profile of stem cell-derived cardiomyocytes matches with the functional complexity of mature cardiomyocytes. This is currently not the case. We are interested in gaining ...
The regenerative potential of the adult heart is very limited and insufficient to replace damaged muscle mass in the diseased heart. Recent advances in cardiac cell therapy and tissue engineering fuel new hope for the development of novel therapeutic approaches with the aim to trigger myocardial regeneration after injury. Stem cell-derived cardiomyocytes represent ideal candidates for cardiac cell-based therapeutic strategies, and current research focuses on the development of cardiac constructs for implantation. Despite the cardiogenic properties of the newly generated cardiomyocytes, these cells present a heterogeneous and immature phenotype, which is more comparable with cardiomyocytes of early developmental stages. However, successful employment of these new cardiomyocytes for myocardial repair demands that the physiological profile of stem cell-derived cardiomyocytes matches with the functional complexity of mature cardiomyocytes. This is currently not the case. We are interested in gaining ...
Genetic regulation of the cell fate transition from lateral plate mesoderm to the specification of cardiomyocytes requires suppression of Wnt/β-catenin signaling, but the mechanism for this is not well understood. By analyzing gene expression and chromatin dynamics during directed differentiation of human embryonic stem cells (hESCs), we identified a suppressor of Wnt/β-catenin signaling, transmembrane protein 88 (TMEM88), as a potential regulator of cardiovascular progenitor cell (CVP) specification. During the transition from mesoderm to the CVP, TMEM88 has a chromatin signature of genes that mediate cell fate decisions, and its expression is highly upregulated in advance of key cardiac transcription factors in vitro and in vivo. In early zebrafish embryos, tmem88a is expressed broadly in the lateral plate mesoderm, including the bilateral heart fields. Short hairpin RNA targeting of TMEM88 during hESC cardiac differentiation increases Wnt/β-catenin signaling, confirming its role as a ...
To the Editor:. We read with interest the article by Hosoda et al,1 Human Cardiac Stem Cell Differentiation Is Regulated by a Mircrine Mechanism. We are pleased to read that Hosoda et al were able to confirm our observations that miR-499 is involved in the differentiation of human cardiac-derived progenitor cells.2. Hosoda and colleagues acknowledged our previous observations in human cardiomyocyte progenitor cells (hCMPCs), but claimed that these cells were erroneously considered a class of cardiac progenitor cells. The authors suggest that our results demonstrated that miR-1 and 499 favor a more mature phenotype in fetal-neonatal cardiomyocytes. Although controversy still exists about different populations of progenitor and stem cells in the heart, we used an exceptionally profound characterized and well-documented cell population,3-5 both present in the fetal and adult human myocardium. hCMPCs do express progenitor markers and early cardiomyocyte-specific transcription factors, but not any ...
TY - JOUR. T1 - The role of the tumor suppressor gene p53 in cardiomyocyte apoptosis. AU - Crow, Michael T.. AU - Long, Xilin. AU - Guglielmi, Mario B.. AU - Asai, Toshinobu. AU - Lakatta, Edward G.. PY - 1998/1/1. Y1 - 1998/1/1. N2 - The possibility that a significant fraction of cardiac myocyte loss in various disease states occurs through apoptosis has elicited considerable attention in recent years. Evidence from human studies as well as in vitro and animal models of disease has shown that cardiac myocyte apoptosis can be induced by a variety of stimuli and in a number of disease states, including hypoxia, ischemia-reperfusion, myocardial infarction, mechanical stretch, aortic constriction, and heart failure. Because adult cardiac myocytes are terminally differentiated cells, the effects of such loss can never be fully compensated. Interest in cardiomyocyte apoptosis has been fueled by the possibility that once the proximal and distal signals were defined that initiate this pathway of cell ...
Fingerprint Dive into the research topics of Generation of reentrant arrhythmias by dominant-negative inhibition of connexin43 in rat cultured myocyte monolayers. Together they form a unique fingerprint. ...
Adult zebrafish possess a significant ability to regenerate injured heart tissue through proliferation of pre-existing cardiomyocytes, which contrasts with the inability of mammals to do so after the immediate postnatal period. Zebrafish therefore provide a model system in which to study how an injured heart can be repaired. However, it remains unknown what important processes cardiomyocytes are involved in other than partial de-differentiation and proliferation. Here we show that migration of cardiomyocytes to the injury site is essential for heart regeneration. Ventricular amputation induced expression of cxcl12a and cxcr4b, genes encoding a chemokine ligand and its receptor. We found that cxcl12a was expressed in the epicardial tissue and that Cxcr4 was expressed in cardiomyocytes. We show that pharmacological blocking of Cxcr4 function as well as genetic loss of cxcr4b function causes failure to regenerate the heart after ventricular resection. Cardiomyocyte proliferation was not affected ...
Accumulating evidence supports the notion that the renin-angiotensin system exists not only in the blood circulation but also in cardiac tissues.34 35 Recently, it has been reported that Ang II induces hypertrophy of cultured cardiac myocytes from neonatal rats9 and embryonic chick8 and also causes the proliferation of cultured neonatal rat cardiac fibroblasts.9 Furthermore, very recently, using an in vitro model of load (stretch)-induced cardiac hypertrophy, Sadoshima et al10 have obtained evidence showing that mechanical stretch leads to release of Ang II from neonatal rat ventricular myocytes and the released Ang II acts as an initial mediator of the stretch-induced hypertrophic response. All these findings, obtained by in vitro studies,8 9 10 support the notion that autocrine release of Ang II from cardiac myocytes is involved in load (stretch)-induced growth of ventricular myocytes, thereby suggesting the central role of Ang II in cardiac hypertrophy and remodeling. However, it remains to ...
Author summary A molecular understanding of cardiomyocyte development is an essential goal for improving clinical approaches to CHD. While TBX20 is an essential transcription factor for heart development and its disease relevance is well established, many fundamental questions remain about the mechanism of TBX20 function. Principle among these is how TBX20 mutations associated with adult dilated cardiomyopathy circumvent (DCM) the essential embryonic requirement for TBX20 in heart development. Here we report using an integrated approach that TBX20 complexes with the cardiac transcription factor CASZ1 in vivo. We confirmed TBX20 and CASZ1 interact biochemically and genetically, and show mice heterozygous for both Tbx20 and Casz1 die, beginning at 4 to 8 weeks post birth, exhibiting hallmarks of DCM. Interestingly, the human mutant TBX20F256I bypasses the early essential requirement for TBX20 but leads to DCM. We report here that TBX20F256I disrupts the TBX20-CASZ1 interaction, ascribing clinical
Cardiac structure and functionare commonly studied using primary culture of neonatal and adult cardiac myocyte. However, their inability to divide and retain their differentiated phenotype in culture limits their use.. Established from a mouse atrial myocyte tumour, HL-1 cells share similar characteristics with primary cultures of cardiac myocytes. They have the ability to proliferate while keeping a differentiated cardiomyocyte phenotype in culture (this allows the use of specific molecular tools as RNA interference). However, there are concerns about their genetic stability and some studies have shown the cells to contain a functionally heterogeneous population.. The team from Imperial College isolated homogeneous and stable clones of HL-1 cell lines - thereby excluding any differences due to cellular heterogeneity of the original cell line - that display phenotypic characteristics consistent with cardiac cells.. Clones 3 and 6 appear to be most promising for cardiac research. These cells ...
Cell proliferation is regulated by the balance between cyclin-dependent kinases (CDKs) and CDK inhibitors such as p27. In neonatal cardiomyocytes, p27 is a key inhibitor of cell proliferation (6) and cyclin D1 is important for cell cycle progression (36). To delineate the pathway through which TIMP-3 inhibits neonatal cardiomyocyte proliferation, the effect of TIMP-3 on cyclin D1 and p27 expression was investigated. Our data showed that cyclin D1 was increased in TIMP-3−/− cardiomyocytes and decreased in rTIMP-3-treated cells as compared with WT. Consistent with these results, p27 expression was decreased in the TIMP-3−/− cardiomyocytes and neonatal hearts as compared with WT. This decrease in p27 expression resulted in an increase in cardiomyocyte proliferation both in vitro and in vivo. Furthermore, treatment of cardiomyocytes with rTIMP-3 resulted in a significant increase in p27 expression, which led to a significant decrease in cardiomyocyte proliferation. Our data suggest that ...
It is believed that in embryonic cardiomyocytes the myocardial contraction is predominantly dependent on transsarcolemmal Ca2+ influx (26, 36). Therefore, it is expected that in embryonic cardiomyocytes, NCX might be a prominent Ca2+ remover and even more important than SERCA. However, it has been recently shown that in murine embryonic cardiomyocytes 8.5-9.5 days old, the majority of Ca2+ removal (∼74%) is accomplished by SERCA (32). The studies on mESCMs showed that the SERCA is the major Ca2+ remover in 17-day-old mESCMs (16). Here, we provided evidence showing that the contribution of SERCA to Ca2+ removal is upregulated with the time of mESCMs differentiation, accompanied with a downregulation of NCX to Ca2+ removal, a similar pattern as reported by Kapur and Banach (16). The functional changes with differentiation also coincide with the gene expression pattern of SERCA and NCX during embryonic development (21, 32) or mESCMs differentiation (12). Moreover, our data demonstrated that ...
We appreciate the interest of Drs Li and Shen in our study,1 which emphasizes the critical role that the insulin-like growth factor-1 (IGF-1) and IGF-1 receptor system has in defining the growth properties of human cardiac stem cells (hCSCs). We shared their view that IGF-1 positively interferes with the consequences of diabetes mellitus and dyslipidemia, and possibly with other cardiovascular pathologies. Based on our interest in IGF-1, a transgenic mouse model with cardiomyocyte-restricted overexpression of IGF-1 was developed.2 With this strategy, an increase in the number of ventricular myocytes was obtained, resulting in a significantly lower systolic and diastolic stress at the cellular level, together with an enhanced ability of the myocardium to sustain increases in pressure or volume loads.. Overexpression of IGF-1 prevents the manifestation of the diabetic myopathy and is associated with a better survival rate of the animals,3 consistent with the observations collected in the ...
Previous studies have reported that immature cardiomyocytes have characteristics of Ca2+-regulatory proteins which are different from that of mature cardiomyocytes [22-25]. During normal cardiac development in rabbits and rats, NCX expression is maximal near the time of birth and then declines postnatally [22, 25]. Conversely, SERCA2a expression levels increased during this period [23-25]. The characteristics of Ca2+-regulatory proteins in immature cardiomyocytes during hypertrophy with or without hypoxia has not been studied extensively, however the results of research will be beneficial for choosing an optimal time of therapy and interpreting the development process of cardiomyocytes in children with CHD.. To our knowledge, this study could be the first effort specifically dedicated to the evaluation of the gene and protein expression of Ca2+-regulatory proteins on human immature cardiomyocytes from RV. There were three major findings in this study. We found that SERCA2a, as a key regulator of ...
TY - JOUR. T1 - Targeted Sprouty1 overexpression in cardiac myocytes does not alter myocardial remodeling or function. AU - Charles, Nathan J.. AU - Huebert, Robert C.. AU - Lee, Sangjin. AU - Adhikari, Neeta. AU - Polster, Sean. AU - Rider, James E.. AU - Braunlin, Elizabeth. AU - Mariash, Ami. AU - Robledo, Maggie. AU - Schuweiler, David. AU - Hall, Jennifer L.. PY - 2010/9/1. Y1 - 2010/9/1. N2 - The mitogen activated protein kinase (MAPK) signaling pathway regulates multiple events leading to heart failure including ventricular remodeling, contractility, hypertrophy, apoptosis, and fibrosis. The regulation of conserved intrinsic inhibitors of this pathway is poorly understood. We recently identified an up-regulation of Sprouty1 (Spry1) in a targeted approach for novel inhibitors of the MAPK signaling pathway in failing human hearts following reverse remodeling. The goal of this study was to test the hypothesis that up-regulated expression of Spry1 in cardiac myocytes would be sufficient to ...
The findings herein advance a strategy for inducing myocardial repair in pediatric patients. Myocardial regeneration experiments in neonatal mice were not feasible until the recent introduction of techniques for inducing myocardial injury (15, 17, 41). LAD ligation (16, 17) and amputation injury (15, 42) in neonatal mice were reported to lead to scarless repair, although these results are controversial (43, 44). Here, we verify that cryoinjury is a technically feasible method that produces scar formation and dysfunction, which is in line with the scar formation and delayed repair process observed in zebrafish (31-33) and neonatal mice (35, 36) after cryoinjury. We also show that cryoinjury in neonatal mice is a useful model for human infants with heart disease because it recapitulates the scar formation, dysfunction, and decrease in cardiomyocyte cell cycle activity frequently seen in young patients with heart disease. The observed decrease in cardiomyocyte proliferation after cryoinjury ...
Lijun Liu is the author of these articles in the Journal of Visualized Experiments: A Model for Perineural Invasion in Head and Neck Squamous Cell Carcinoma, Isolation and Culture of Adult Mouse Cardiomyocytes for Cell Signaling and in vitro Cardiac Hypertrophy
In the studies reported in the American Journal of Pathology, Dr. Charles Murry and his colleagues at the University of Washington, in collaboration with scientists at Geron Corporation, produced cardiomyocytes from hESCs and injected the cells into the left ventricular wall of normal healthy rats. The transplant was examined one and four weeks after injection and human cells were detected in the rat myocardium at both timepoints. At the four week timepoint, the grafted human cardiomyocytes were identified using characteristic markers including sarcomeric actin, alpha and beta-myosin heavy chain, and myosin light chain 2v. Approximately 10% of the cardiomyocytes at the four week timepoint retained proliferative capacity, thereby potentially enhancing engraftment. Both host and graft derived angiogenesis (new blood vessel formation) was observed, critical to sustaining the viability of the graft. No evidence of tumor formation was seen ...
This method - tested in a mouse heart attack model - doubled the engraftment rate of injected stem cell-derived cardiomyocytes. Ram KannappanThe heart cannot regenerate muscle tissue after a heart attack has killed part...
Activation of mammalian sterile 20-like kinase 1 (Mst1) by genotoxic compounds is known to stimulate apoptosis in some cell types. The importance of Mst1 in cell death caused by clinically relevant pathologic stimuli is unknown, however. In this study, we show that Mst1 is a prominent myelin basic protein kinase activated by proapoptotic stimuli in cardiac myocytes and that Mst1 causes cardiac myocyte apoptosis in vitro in a kinase activity-dependent manner. In vivo, cardiac-specific overexpression of Mst1 in transgenic mice results in activation of caspases, increased apoptosis, and dilated cardiomyopathy. Surprisingly, however, Mst1 prevents compensatory cardiac myocyte elongation or hypertrophy despite increased wall stress, thereby obscuring the use of the Frank-Starling mechanism, a fundamental mechanism by which the heart maintains cardiac output in response to increased mechanical load at the single myocyte level. Furthermore, Mst1 is activated by ischemia/reperfusion in the mouse heart ...
Francis J. Manasek; THE APPEARANCE OF GRANULES IN THE GOLGI COMPLEX OF EMBRYONIC CARDIAC MYOCYTES . J Cell Biol 1 December 1969; 43 (3): 605-610. doi: Download citation file:. ...
Human Cardiomyocyte Perfusion Serum Free Media. This Product is also available with Serum Cat# P36044-15S This product would require and Human Cardiomyocytes Cat# 36044-15 This product is tissue culture tested including Stem Cells and is.... ...
TY - JOUR. T1 - Heterogeneity of T-Tubules in Pig Hearts. AU - Gadeberg, Hanne C. AU - Bond, Richard C. AU - Kong, Cherrie. AU - Chanoit, Guillaume. AU - Ascione, Raimondo. AU - Cannell, Mark. AU - James, Andrew. PY - 2016/6/9. Y1 - 2016/6/9. N2 - BackgroundT-tubules are invaginations of the sarcolemma that play a key role in excitation-contraction coupling in mammalian cardiac myocytes. Although t-tubules were generally considered to be effectively absent in atrial myocytes, recent studies on atrial cells from larger mammals suggest that t-tubules may be more numerous than previously supposed. However, the degree of heterogeneity between cardiomyocytes in the extent of the t-tubule network remains unclear. The aim of the present study was to investigate the t-tubule network of pig atrial myocytes in comparison with ventricular tissue.MethodsCardiac tissue was obtained from young female Landrace White pigs (45-75 kg, 5-6 months old). Cardiomyocytes were isolated by arterial perfusion with a ...
Cardiac cells are subjected to mechanical load during each heart-beat. Normal heart load is essential for physiological development and cardiac function. At the same time, excessive load can induce pathologies such as cardiac hypertrophy. While the forces working on the heart as an organ are well-understood, information regarding stretch response at the cellular level is limited. Since cardiac stretch-response depends on the amplitude and pattern of the applied load as well as its timing during the beating cycle, the directionality of load application and its phase relative to action potential generation must be controlled precisely. Here, we design a new experimental setup, which enables high-resolution fluorescence imaging of cultured cardiac cells under cyclic uniaxial mechanical load and electrical stimulation. Cyclic stretch was applied in different phases relative to the electrical stimulus and the effect on cardiac cell beating was monitored. The results show a clear phase-dependent response and
This study was initiated with the original aim of assessing the consequences of the expression of the functional α2-subunit of the rat Na+-K+-ATPase in the neonatal rat cardiac myocytes lacking this isoform. It soon became evident, however, that only a truncated α2-subunit not likely to be functional was overexpressed in these cells. Because enzyme and receptor fragments may often act like inactive mutant variants and cause dominant negative inhibition (2, 10, 12, 23, 27, 36) we attempted to determine whether the expression of the α2-fragment impaired the function of endogenous Na+-K+-ATPase in the neonatal myocytes. Our findings clearly show that the ion transport function of Na+-K+-ATPase is indeed inhibited concomitant with the expression of the truncated α2-isoform and that this is accompanied by a significant reduction of the α1-protein content of the neonatal myocyte. Because the induced reduction of the α3-protein content is small, if any, and because it is established that α1 ...
Heart attacks are a leading cause of mortality in the United States, responsible for over 500,000 deaths annually. Despite advancing treatments for acute heart attack, 5-year mortality exceeds 50% as the organ fails to heal the resulting scar. Recent studies revealed modest cardiac regeneration occurring throughout life and accelerating (albeit insufficiently) post-injury. However, the magnitude is contested with some studies indicating low cardiomyocyte formation and others indicating rapid formation of increasingly inferior cardiomyocytes. Resolving this question determines the needed strategy for repair augmentation. Chapter 3 scrutinizes current apparently-paradoxical studies and offers a unified estimate of cardiomyocyte turnover via a hybrid-model software platform. As limited engraftment (|2%) was cited as a primary impediment in bone marrow cell (BMC) infusion clinical trials, Chapter 4 recapitulates these trials in an intact-organ murine model--the isolated perfused heart. Flow cytometry
Tissue regeneration without tumor formation may soon be within reach, at least for heart repair. On page 405, Behfar et al. report that embryonic stem (ES) cells preprogrammed to mature into cardiomyocytes can fix injured hearts in vivo without seeding tumors.. Directing ES cells to become a particular tissue type in vivo is an inefficient process. Consequently, transplanted ES cell populations may give rise to tumors in recipient hosts. Behfar et al. reasoned that delivery of partially differentiated ES cells may result in safe outcome provided that a modulator of differentiation shuts down troublesome tumor pathways.. When ES cells are delivered in vivo, their tumorigenicity is reduced in mice that suffer heart attacks. This is associated with TNF production. But TNF had not been tested for its ability to direct cardiomyocyte differentiation, although ES cells do express receptors for TNF. So the authors wondered whether TNF-driven signaling would be enough to guide cells into a ...
J:169706 Abdul-Ghani M, Dufort D, Stiles R, De Repentigny Y, Kothary R, Megeney LA, Wnt11 promotes cardiomyocyte development by caspase-mediated suppression of canonical Wnt signals. Mol Cell Biol. 2011 Jan;31(1):163-78 ...
Yetişkin, kardiyak miyositler hayvan kalpleri izole edilebilir ve birkaç gün kültüre temel hücrelerdir. Bu kültür süre içinde...
The heat shock proteins (HSP) are a highly conserved family of proteins with critical functions in protein folding, protein trafficking, and cell signaling. These proteins also protect the cell against injury. HSP60 has been found in the extracellular space and has been identified in the plasma of s …
TY - JOUR. T1 - Non-cell autonomous cues for enhanced functionality of human embryonic stem cell-derived cardiomyocytes via maturation of sarcolemmal and mitochondrial K ATP channels. AU - Keung, Wendy. AU - Ren, Lihuan. AU - Sen Li, Li. AU - Wong, Andy On Tik. AU - Chopra, Anant. AU - Kong, Chi Wing. AU - Tomaselli, Gordon F.. AU - Chen, Christopher S.. AU - Li, Ronald A.. PY - 2016/9/28. Y1 - 2016/9/28. N2 - Human embryonic stem cells (hESCs) is a potential unlimited ex vivo source of ventricular (V) cardiomyocytes (CMs), but hESC-VCMs and their engineered tissues display immature traits. In adult VCMs, sarcolemmal (sarc) and mitochondrial (mito) ATP-sensitive potassium (K ATP) channels play crucial roles in excitability and cardioprotection. In this study, we aim to investigate the biological roles and use of sarcK ATP and mitoK ATP in hESC-VCM. We showed that SarcI K, ATP in single hESC-VCMs was dormant under baseline conditions, but became markedly activated by cyanide (CN) or the known ...
TY - JOUR. T1 - N-cadherin overexpression enhances the reparative potency of human-induced pluripotent stem cell-derived cardiac myocytes in infarcted mouse hearts. AU - Lou, Xi. AU - Zhao, Meng. AU - Fan, Chengming. AU - Fast, Vladimir G.. AU - Valarmathi, Mani T.. AU - Zhu, Wuqiang. AU - Zhang, Jianyi. N1 - Funding Information: This work was supported by the National Institute of Health (NHLBI R01 grants: HL95077, HL114120, HL131017, and UO1 HL 134764) for J.Z. Publisher Copyright: © 2019 Published on behalf of the European Society of Cardiology. All rights reserved.. PY - 2020/3/1. Y1 - 2020/3/1. N2 - Aims: In regenerative medicine, cellular cardiomyoplasty is one of the promising options for treating myocardial infarction (MI); however, the efficacy of such treatment has shown to be limited due to poor survival and/or functional integration of implanted cells. Within the heart, the adhesion between cardiac myocytes (CMs) is mediated by N-cadherin (CDH2) and is critical for the heart to ...
Cardiomyocytes derived from human embryonic stem cells (hESC-CMs) can improve the contractility of injured hearts. We hypothesized that mesodermal cardiovascular progenitors (hESC-CVPs), capable of generating vascular cells in addition to cardiomyocytes, would provide superior repair by contributing to multiple components of myocardium. We performed a head-to-head comparison of hESC-CMs and hESC-CVPs and compared these with the most commonly used clinical cell type, human bone marrow mononuclear cells (hBM-MNCs). In a nude rat model of myocardial infarction, hESC-CMs and hESC-CVPs generated comparable grafts. Both similarly improved systolic function and ventricular dilation. Furthermore, only rare human vessels formed from hESC-CVPs. hBM-MNCs attenuated ventricular dilation and enhanced host vascularization without engrafting long-term or improving contractility. Thus, hESC-CMs and CVPs show similar efficacy for cardiac repair, and both are more efficient than hBM-MNCs. However, hESC-CVPs do ...
Field potential duration (FPD) in human-induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs), which can express QT interval in an electrocardiogram, is reported to be a useful tool to predict K{sup +} channel and Ca{sup 2+} channel blocker effects on QT interval. However, there is no report showing that this technique can be used to predict multichannel blocker potential for QT prolongation. The aim of this study is to show that FPD from MEA (Multielectrode array) of hiPS-CMs can detect QT prolongation induced by multichannel blockers. hiPS-CMs were seeded onto MEA and FPD was measured for 2 min every 10 min for 30 min after drug exposure for the vehicle and each drug concentration. I{sub Kr} and I{sub Ks} blockers concentration-dependently prolonged corrected FPD (FPDc), whereas Ca{sup 2+} channel blockers concentration-dependently shortened FPDc. Also, the multichannel blockers Amiodarone, Paroxetine, Terfenadine and Citalopram prolonged FPDc in a concentration dependent manner. ...
In spite of serious cardiotoxicity side-effects, doxorubicin is frequently used for treatment of several types of cancers. Isolated human adult cardiomyocytes could be the best model for assessing drug-induced cardiotoxicity, while harvesting mature cardiomyocytes is restricted by some limitations such as biopsy size, cell numbers, viability, proliferative capacity and their disability to be passaged as a cell line. In the present study, human embryonic stem cell (hESC)-derived cardiomyocytes applied as a model for evaluation of doxorubicin cardiotoxicity. In this process, cardiogenic differentiated hESCs spheroids were exposed to different concentrations of doxorubicin for 24, 48 and 72 hours. The viability of spheroids as well as their morphology was assessed as important criterion of cardiotoxicity. Findings of the study showed that the viability of spheroids was significantly reduced at doses of 3 and 30 µM (P|0.05). Moreover, cell morphology was changed in the presence of same doses. Overall
Human embryonic stemcells (hESCs) can serve as a potentially limitless source of cells that may enable regeneration of diseased tissue and organs. Here we investigate the use of human embryonic stemcell-derived cardiomyocytes (hESC-CMs) in promoting recovery from cardiac ischemia reperfusion injury in a mouse model. Using microarrays, we have described the hESC-CM transcriptome within the spectrum of changes that occur between undifferentiated hESCs and fetal heart cells. The hESC-CMs expressed cardiomyocyte genes at levels similar to those found in 20-week fetal heart cells, making this population a good source of potential replacement cells in vivo. Echocardiographic studies showed significant improvement in heart function by 8 weeks after transplantation. Finally, we demonstrate long-term engraftment of hESC-CMs by using molecular imaging to track cellular localization, survival, and proliferation in vivo. Taken together, global gene expression profiling of hESC differentiation enables a ...
Peppiatt CM, Collins TJ, Mackenzie L et al. 2-Aminoethoxydiphenyl borate (2-APB) antagonises inositol 1,4,5-trisphosphate-induced calcium release, inhibits calcium pumps and has a use-dependent and slowly reversible action on store-operated calcium entry channels. Cell Calcium 2003; 34:97-108 ...
What is new in cardiomyocyte necrosis? Read our cardiomyocyte necrosis blog and learn more about the cardiomyocyte necrosis treatments on Medical Writer Agency | 醫學作家香港 | 醫學寫作 | MediPR | MediPaper Hong Kong.
Cardiogenesis processes in human and animals have differential dynamics, suggesting the existence of species-specific regulators during heart development. However, it remains a challenge to discover the human-specific cardiac regulatory genes, given that most coding genes are conserved. Here, researchers at the University of Pittsburgh School of Medicine report the identification of a human-specific long noncoding RNA, Heart Brake LncRNA 1 (HBL1), which regulates cardiomyocyte development from human induced pluripotent stem cells (hiPSCs). Overexpression of HBL1 repressed, whereas knockdown and knockout of HBL1 increased, cardiomyocyte differentiation from hiPSCs. HBL1 physically interacted with MIR1 in an AGO2 complex. Disruption of MIR1 binding sites in HBL1 showed an effect similar to that of HBL1 knockout. SOX2 bound to HBL1 promoter and activated its transcription. Knockdown of SOX2 in hiPSCs led to decreased HBL1 expression and increased cardiomyocyte differentiation efficiency. Thus, HBL1 ...
TY - JOUR. T1 - Functional role of M-type (KCNQ) K+ channels in adrenergic control of cardiomyocyte contraction rate by sympathetic neurons. AU - Zaika, Oleg. AU - Zhang, Jie. AU - Shapiro, Mark S. PY - 2011/5. Y1 - 2011/5. N2 - M-type (KCNQ) K+ channels are known to regulate excitability and firing properties of sympathetic neurons (SNs), but their role in regulating neurotransmitter release is unclear, requiring further study. We sought to use a physiological preparation in which SNs innervate primary cardiomyocytes to evaluate the direct role of M-channels in the release of noradrenaline (NA) from SNs. Co-cultures of rat SNs and mouse cardiomyocytes were prepared, and the contraction rate (CR) of the cardiomyocyte syncytium monitored by video microscopy. We excited the SNs with nicotine, acting on nicotinic acetylcholine receptors, and monitored the increase in CR in the presence or absence of the specific M-channel opener retigabine, or agonists of bradykinin B2 or purinergic P2Y receptors ...
Given the poor track record to date of animal models for creating cardioprotective drugs, human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) have been proposed as a therapeutically relevant human platform to guide target validation and cardiac drug development. Mitogen-Activated Protein Kinase Kinase Kinase Kinase-4 (MAP4K4) is an upstream member of the MAPK superfamily that is implicated in human cardiac muscle cell death from oxidative stress, based on gene silencing and pharmacological inhibition in hPSC-CMs. A further role for MAP4K4 was proposed in heart muscle cell death triggered by cardiotoxic anti-cancer drugs, given its reported activation in failing human hearts with doxorubicin (DOX) cardiomyopathy, and its activation acutely by DOX in cultured cardiomyocytes. Here, we report successful protection from DOX in two independent hPSC-CM lines, using two potent, highly selective MAP4K4 inhibitors. The MAP4K4 inhibitors enhanced viability and reduced apoptosis at otherwise ...
TY - JOUR. T1 - Lycopene inhibits urotensin-II-induced cardiomyocyte hypertrophy in neonatal rat cardiomyocytes. AU - Chao, Hung Hsing. AU - Sung, Li-Chin. AU - Chen, Cheng Hsien. AU - Liu, Ju Chi. AU - Chen, Jin Jer. AU - Cheng, Tzu-Hurng. PY - 2014. Y1 - 2014. N2 - This study investigated how lycopene affected urotensin-II- (U-II-) induced cardiomyocyte hypertrophy and the possible implicated mechanisms. Neonatal rat cardiomyocytes were exposed to U-II (1 nM) either exclusively or following 6 h of lycopene pretreatment (1-10 μM). The lycopene (3-10 μM) pretreatment significantly inhibited the U-II-induced cardiomyocyte hypertrophy, decreased the production of U-II-induced reactive oxygen species (ROS), and reduced the level of NAD(P)H oxidase-4 expression. Lycopene further inhibited the U-II-induced phosphorylation of the redox-sensitive extracellular signal-regulated kinases. Moreover, lycopene treatment prevented the increase in the phosphorylation of serine-threonine kinase Akt and ...
Laminins form a large family of extracellular matrix (ECM) proteins, and their expression is a prerequisite for normal embryonic development. Herein we investigated the role of the laminin gamma1 chain for cardiac muscle differentiation and function using cardiomyocytes derived from embryonic stem c …
G-protein-coupled receptor agonists are powerful stimulators of mitogen-activated protein kinase (MAPK) cascades in cardiac myocytes. However, little is known regarding the physiological activation of enzymes downstream of MAPKs. We examined the activation of mitogen- and stress-activated protein kinase-1 (MSK1), a downstream target of MAPKs, in adult rat cardiac myocytes by phenylephrine and endothelin-1. Both agonists induced the phosphorylation of MSK1 at Thr-581 and Ser-376 but not at Ser-360. Maximal phosphorylation was observed at 10-15min after stimulation and it correlated with increased activity. Maximal activation of MSK1 in adult cardiomyocytes temporally coincided with maximal p38 MAPK activation while activation of the extracellular-signal-regulated kinase (ERK) cascade was more rapid. Phosphorylation and activation of MSK1 was completely inhibited by either PD98059 (ERK1/2 pathway inhibitor) or SB203580 (p38 MAPK inhibitor) alone. These data demonstrate that MSK1 activation in ...
Although functions of MR in several other cell types have been elucidated in pathologic cardiac hypertrophy and heart failure,15-17,19,36-38 the roles of MR in T cells have not been illuminated. Through this study, we demonstrated that eplerenone and TMRKO attenuated POL-induced cardiac remodeling and dysfunction in parallel with attenuated cardiac inflammation, as well as decreased T-cell accumulation and activation in the heart. Moreover, in vitro results illustrated direct regulation of T-cell activation by MR.. This study implies that MR blockade in T cells is a feasible approach to treat pathologic cardiac hypertrophy and heart failure. MR deficiency in T cells was sufficient to suppress POL-induced cardiac hypertrophy, cardiac fibrosis, and cardiac dysfunction, as well as cardiac inflammation in mice. Particularly, TMRKO completely abrogated parts of the phenotype 1 week after POL, indicating that MR in T cells may be more important than MR in other cellular compartments in the early stage ...
Kolacsek, Orsolya and Pergel, Enikő and Varga, Nóra and Apáti, Ágota and Orbán, Tamás I. (2017) Ct shift: A novel and accurate real-time PCR quantification model for direct comparison of different nucleic acid sequences and its application for transposon quantifications. GENE, 598. pp. 43-49. ISSN 0378-1119 Apáti, Ágota and Berecz, Tünde and Sarkadi, Balázs (2016) Calcium signaling in human pluripotent stem cells. Cell Calcium, 59 (2-3). pp. 117-123. ISSN 0143-4160 Pálóczi, János and Varga, Zoltán V. and Apáti, Ágota and Szebényi, Kornélia and Sarkadi, Balázs and Csont, Tamás Bálint and Ferdinandy, Péter and Görbe, Anikó (2016) Exogenous Nitric Oxide Protects Human Embryonic Stem Cell-Derived Cardiomyocytes against Ischemia/Reperfusion Injury. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2016. pp. 1-10. ISSN 1942-0900 Sándor, Sára Anna and Jordanidisz, T. and Schamberger, Anita and Várady, György and Erdei, Zsuzsa and Apáti, Ágota and Sarkadi, Balázs and Orbán, ...
Background: MiR-499 is a cardiac-abundant miRNA. However, the biological functions of miR-499 in differentiated cardiomyocytes or in the cardiomyocyte differentiation process is not very clear. Sox6 is believed to be one of its targets, and is also believed to play a role in cardiac differentiation. Therefore, our aim was to investigate the association between Sox6 and miR-499 during cardiac differentiation.. Methodology/Principal Findings: Using a well-established in vitro cardiomyocyte differentiation system, mouse P19CL6 cells, we found that miR-499 was highly expressed in the late stage of cardiac differentiation. In cells stably transfected with miR-499 (P-499 cells), it was found that miR-499 could promote the differentiation into cardiomyocytes at the early stage of cardiac differentiation. Notably, cell viability assay, EdU incorporation assay, and cell cycle profile analysis all showed that the P-499 cells displayed the distinctive feature of hyperplastic growth. Further investigation ...
Intracellular Ca2+ overload induced by extracellular Ca2+ entry has previously been confirmed to be an important mechanism for the cardiotoxicity as well as the acute heart dysfunction induced by jellyfish venom, while the underlying mechanism remains to be elucidated. Under extracellular Ca2+-free or Ca2+-containing conditions, the Ca2+ fluorescence in isolated adult mouse cardiomyocytes pre-incubated with tentacle extract (TE) from the jellyfish Cyanea capillata and β blockers was scanned by laser scanning confocal microscope. Then, the cyclic adenosine monophosphate (cAMP) concentration and protein kinase A (PKA) activity in primary neonatal rat ventricular cardiomyocytes were determined by ELISA assay. Furthermore, the effect of propranolol against the cardiotoxicity of TE was evaluated in Langendorff-perfused rat hearts and intact rats. The increase of intracellular Ca2+ fluorescence signal by TE was significantly attenuated and delayed when the extracellular Ca2+ was removed. The β adrenergic
Intramyocardial injections of cultured fetal cardiomyocytes after infarction in female rats in an ischaemia-reperfusion model increased ejection fraction at one month; male cells transplanted into the female hosts were identified at necropsy by detection of the Y chromosome using an in situ hybridisation technique.7 In a mouse model of doxorubicin induced global cardiomyopathy,8 local transplantation of fetal cardiomyocytes can also improve global function, suggesting the intervention of paracrine factors. Comparing intramyocardial injections of cultured fetal cardiomyocytes and allogenic fetal skeletal myoblasts after infarction in rats,9 the functional equivalence of these two types of cells was demonstrated with decreased cavity dilatation and increased ejection fraction of similar magnitude; this anti-remodelling effect was more pronounced for the lowest ejection fractions (, 40%) with an approximately 30% relative increase in ejection fraction without cavity dilatation. Similar results ...
After myocardial infarction in the mammalian heart, millions of cardiomyocytes are lost and replaced by fibrotic scar tissue. While fibrosis is persistent in adult mammals, there are some vertebrates, including zebrafish, with the capacity for regeneration. This process does not occur in the absence of fibrosis. Here we studied subpopulations of collagen-producing cells and analyzed their fate after complete regeneration of the zebrafish myocardium. Our data show that fibroblasts persisted in the regenerated heart but shut down the profibrotic program. While fibrosis could be considered as detrimental to the regeneration process, our study reveals a positive effect on cardiomyocyte proliferation. Accordingly, a fibrotic response can be beneficial for heart regeneration. In the zebrafish (Danio rerio), regeneration and fibrosis after cardiac injury are not mutually exclusive responses. Upon cardiac cryoinjury, collagen and other extracellular matrix (ECM) proteins accumulate at the injury site. However,
Control of cardiomyocyte cytosolic Ca(2+) levels is crucial in determining inotropic status and ischemia/reperfusion stress response. Responsive to fluctuations in cellular Ca(2+), Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is a serine/threonine kinase integral to the processes regulating cardiomyocyte Ca(2+) channels/transporters. CaMKII is primarily expressed either in the δB or δC splice variant forms, which may mediate differential influences on cardiomyocyte function and pathological response mechanisms. Increases in myocyte Ca(2+) levels promote the binding of a Ca(2+)/calmodulin complex to CaMKII, to activate the kinase. Activity is also maintained through a series of post-translational modifications within a critical region of the regulatory domain of the protein. Recent data indicate that the post-translational modification status of CaMKIIδB/δC variants may have an important influence on reperfusion outcomes. This study provided the first evidence that the specific type ...
Methods Male wild type mice were randomly divided into control and PD150606 groups. Mice were subjected to myocardial ischemia by occlusion of the left anterior descending coronary artery for 45 min and reperfusion for 3 h (I/R). Terminal deoxynucleotidyl transferase d-UTP nick end labeling (TUNEL) staining was performed using an In Situ Cell Death Detection kit on paraffin heart sections (5 mm). Hoechst 33342 was used as a counter-stain. Adult mouse cardiomyocytes were isolated and cultured, then subjected to ischemia for 1 h, and reperfusion for 3 h. The survival of cardiomyocytes, activity of calpain and caspase-3, cytoplasmic DNA fragments and cytochrome c concentrations were determined. Results Compared to control, the numbers of TUNEL-positive nuclei were significantly increased in the peri-infarct area in I/R mice (p,0.05). Compared to normal cultured cardiomyocytes, the survival of the cells significantly decreased, however the activation of calpain and caspase-3, and cytoplasmic DNA ...
Cardiac myocytes also possess V1R. Additionally V1R are located in brain, testis, superior cervical ganglion, liver, blood ...
cardiac myocytes. Kir channels close upon depolarization, slowing membrane repolarization and helping maintain a more prolonged ... Kir channels are found in multiple cell types, including macrophages, cardiac and kidney cells, leukocytes, neurons, and ... It is characterized by periodic paralysis, cardiac arrhythmias and dysmorphic features. (See also KCNJ2) ... The process of inward-rectification was discovered by Denis Noble in cardiac muscle cells in 1960s and by Richard Adrian and ...
1998). "Termination of Ca2+ release by a local inactivation of ryanodine receptors in cardiac myocytes". Proc. Natl. Acad. Sci ... 1998). "Termination of Ca2+ release by a local inactivation of ryanodine receptors in cardiac myocytes". Proc. Natl. Acad. Sci ... "Fractional SR Ca release is regulated by trigger Ca and SR Ca content in cardiac myocytes". American Journal of Physiology. ... "T-tubule function in mammalian cardiac myocytes". Circulation Research. 92 (11): 1182-92. doi:10.1161/01.res.0000074908.17214. ...
Kanter HL, Saffitz JE, Beyer EC (1992). "Cardiac myocytes express multiple gap junction proteins". Circ. Res. 70 (2): 438-44. ... Kanter HL, Saffitz JE, Beyer EC (1994). "Molecular cloning of two human cardiac gap junction proteins, connexin40 and ...
They are expressed in skeletal and cardiac myocytes. Troponin T binds to tropomyosin and helps position it on actin, and ... The cardiac subtype of troponin T is especially useful in the laboratory diagnosis of heart attack because it is released into ... Slow skeletal troponin T1, TNNT1 (19q13.4, 191041) Cardiac troponin T2, TNNT2 (1q32, 191045) Fast skeletal troponin T3, TNNT3 ( ... Review Date 10/6/2015 "Development of the Cardiac Troponin T Immunoassay". American Association for Clinical Chemistry, Inc. ...
In cardiac myocytes this forms a scalloped surface. The cytoskeleton is what the rest of the cell builds off of and has two ... "Cardiac muscle tissue". Retrieved 3 May 2021. Myocytes at the US National Library of Medicine Medical Subject Headings (MeSH) " ... A muscle cell also known as a myocyte when referring to a cardiac muscle cell (cardiomyocyte), or a smooth muscle cell as these ... Zhao R, Watt AJ, Battle MA, Li J, Bondow BJ, Duncan SA (May 2008). "Loss of both GATA4 and GATA6 blocks cardiac myocyte ...
Ikeda K, Tojo K, Oki Y, Nakao K (September 2002). "Urocortin has cell-proliferative effects on cardiac non-myocytes". Life ... These effects are likely mediated through the CRF type 2 receptor, as this receptor is found in the cardiac atria and ...
and a block on the differentiation of cardiac myocyte,. both of which lead to embryonic death. Cripto's functions have been ...
2007). "Cyclic nucleotide phosphodiesterase PDE1C1 in human cardiac myocytes". J. Biol. Chem. 282 (45): 32749-57. doi:10.1074/ ...
Huang X, Walker JW (Apr 2004). "Myofilament anchoring of protein kinase C-epsilon in cardiac myocytes". Journal of Cell Science ... Disatnik MH, Buraggi G, Mochly-Rosen D (Feb 1994). "Localization of protein kinase C isozymes in cardiac myocytes". ... PKCε binds and phosphorylates cardiac troponin I (cTnI) and cardiac troponin T (cTnT) in complex with troponin C (cTnC); ... "A selective epsilon-protein kinase C antagonist inhibits protection of cardiac myocytes from hypoxia-induced cell death". The ...
... (Ccna2) is a key protein involved in the direction of mammalian cardiac myocytes to grow and divide, and has been ... Normally, Ccna2 is silenced postnatally in mammalian cardiac myocytes. Because of this gene silencing, adult heart muscle cells ... Delivery of Ccna2 into cardiac tissue invokes a regenerative response and markedly enhances cardiac function. Increased ... Ccna2 mediated cardiac repair showed both a decrease in fibrosis in the peri-infarct tissue and a greater number of ...
Cardiac myocyte renewal has been found to occur in normal adult humans, and at a higher rate in adults following acute heart ... "Evidence that human cardiac myocytes divide after myocardial infarction". The New England Journal of Medicine. 344 (23): 1750-7 ... MRL mice show the same amount of cardiac injury and scar formation as normal mice after a heart attack. However, recent studies ... Even in adult myocardium following infarction, proliferation is only found in around 1% of myocytes around the area of injury, ...
Cohen-Barak O, Yi Z, Hagiwara N, Monzen K, Komuro I, Brilliant MH (2003). "Sox6 regulation of cardiac myocyte development". ...
... reversibly binds to beta adrenergic receptors on cardiac myocytes. Inhibition of these receptors prevents a response ... Reis Filho JR, Cardoso JN, Cardoso CM, Pereira-Barretto AC (June 2015). "Reverse Cardiac Remodeling: A Marker of Better ...
... is expressed at very low levels in cardiac myocytes. Although its presence has been noted in cardiomyocytes of both ... Therefore, minimizing cardiac myostatin may improve cardiac output. Myostatin gene mutations are cited by a Stanford University ... Pathological states that increase cardiac stress and promote heart failure can induce a rise in both cardiac myostatin mRNA and ... in which cardiac myostatin induces whole-body muscular atrophy. Physiologically, minimal amounts of cardiac myostatin are ...
Extensive cardiac necrosis can occur by day three after infection as incubated viruses lyse myocytes, resulting in severe and ... T-cells not only lyse and destroy infected myocytes, but due to molecular mimicry, they also destroy normal, healthy cardiac ... Essentially, sCAR-Fc mimics CAR receptors on cardiac cells, competitively inhibiting viral attachment and entry into myocytes. ... "Coxsackievirus B3 infection leads to cell death of cardiac myocytes". J. Mol. Cell. Cardiol. 26 (7): 907-13. doi:10.1006/jmcc. ...
"Phosphoregulation of the titin-cap protein telethonin in cardiac myocytes". The Journal of Biological Chemistry. 289 (3): 1282- ... Telethonin has a unique β-sheet structure, which enables antiparallel association with the Titin Z1-Z2 domains in cardiac and ... Telethonin is expressed in cardiac and skeletal muscle at Z-discs and functions to regulate sarcomere assembly, T-tubule ... Telethonin expression is developmentally regulated in both cardiac and skeletal muscle and is thought to be critical to ...
Shaw RM, Colecraft HM (May 2013). "L-type calcium channel targeting and local signalling in cardiac myocytes". Cardiovascular ... Powers PA, Gregg RG, Hogan K (Sep 1992). "Linkage mapping of the human gene for the alpha 1 subunit of the cardiac DHP- ... It depolarizes at -30mV and helps define the shape of the action potential in cardiac and smooth muscle. The protein encoded by ... "Assignment of the human gene for the alpha 1 subunit of the cardiac DHP-sensitive Ca2+ channel (CCHL1A1) to chromosome 12p12- ...
Wu F, Yan W, Pan J, Morser J, Wu Q (May 2002). "Processing of pro-atrial natriuretic peptide by corin in cardiac myocytes". The ... Wang W, Cui Y, Shen J, Jiang J, Chen S, Peng J, Wu Q (Nov 2012). "Salt-sensitive hypertension and cardiac hypertrophy in ... Yan W, Wu F, Morser J, Wu Q (Jul 2000). "Corin, a transmembrane cardiac serine protease, acts as a pro-atrial natriuretic ... Yan W, Wu F, Morser J, Wu Q (Jul 2000). "Corin, a transmembrane cardiac serine protease, acts as a pro-atrial natriuretic ...
Nitroxyl has also been shown to increase the sensitivity to cardiac myocytes to Ca2+, which in turn enhances the force of ... Therefore, stimulation of SERCA leads to accelerated uptake of Ca2+ from the cytosol of the cardiac myocyte. Secondly, the ... Sarcoplasmic reticulum CaATPase (SERCA) is an energy-dependent ion pump found the sarcoplasmic reticulum of cardiac myocytes ... "Nitroxyl Activates SERCA in Cardiac Myocytes via Glutathiolation of Cysteine 674". Circulation Research. 104 (6): 720-723. doi: ...
... efficacy as a cardiac differentiation factor because it promotes the transdifferentiation of cardiac cells to skeletal myocytes ... "5-azacytidine promotes the transdifferentiation of cardiac cells to skeletal myocytes". Cellular Reprogramming. 16 (5): 324-30 ...
Cannell MB, Berlin JR, Lederer WJ (1987-01-01). "Intracellular calcium in cardiac myocytes: calcium transients measured using ... The first real time (video rate) Ca2+ imaging was carried out in 1986 in cardiac cells using intensified video cameras. Later ...
In cardiac myocytes, the L-type calcium channel passes inward Ca2+ current and triggers calcium release from the sarcoplasmic ... Shaw RM, Colecraft HM (May 2013). "L-type calcium channel targeting and local signalling in cardiac myocytes". Cardiovascular ... L-type calcium channel blocker drugs are used as cardiac antiarrhythmics or antihypertensives, depending on whether the drugs ... of these channels increases their permeability to calcium and increases the contractility of their respective cardiac myocytes ...
... 1 constitutes the large conductance cation channel of cardiac myocytes. Pannexin 1 and pannexin 2 underlie channel ...
"5-azacytidine promotes the transdifferentiation of cardiac cells to skeletal myocytes". Cellular Reprogramming. 16 (5): 324-330 ... The DNA methylation inhibitor, 5-azacytidine is also known to promote phenotypic transdifferentiation of cardiac cells to ...
Cardiac muscle is found only in the heart, allowing it to contract and pump blood round the body. Nervous tissue is composed of ... Muscle cells (myocytes) form the active contractile tissue of the body. Muscle tissue functions to produce force and cause ... Muscle is formed of contractile filaments and is separated into three main types; smooth muscle, skeletal muscle and cardiac ...
"Specific attachment of desmin filaments to desmosomal plaques in cardiac myocytes". The EMBO Journal. 2 (5): 735-42. doi: ... In cardiac muscle, desmoplakin is localized to intercalated discs which mechanically couple cardiac cells to function in a ... In cardiac muscle, desmoplakin is localized to desmosomes in intercalated discs. Desmoplakin isoform DPI is highly expressed ... DPI is the predominant isoform expressed in cardiac muscle. The DSP gene is located on chromosome 6p24.3, containing 24 exons ...
"Channelopathy as a SUDEP Biomarker in Dravet Syndrome Patient-Derived Cardiac Myocytes". Stem Cell Reports. 11 (3): 626-634. ... Decreased excitation of GABA interneurons can lead to neuronal hyper-excitability and seizures as well as cardiac arrhythmias. ... cardiac arrhythmia, and demyelinating disease. She has played a critical role in using translational research to model and find ...
... integral membrane protein 2 is a novel component of the cardiac intercalated disc and vital for load-induced cardiac myocyte ... "The involvement of adherens junction components in myofibrillogenesis in cultured cardiac myocytes". Development. 114 (1): 173- ... In cardiac muscle, N-cadherin is an integral component in adherens junctions residing at intercalated discs, which function to ... In cardiac muscle, N-cadherin is found at intercalated disc structures which provide end-on cell-cell connections that ...
"Tertiapin potently and selectively blocks muscarinic K+ channels in rabbit cardiac myocytes". The Journal of Pharmacology and ... An inhibition by tertiapin will result in a shorter cardiac action potential with loss of parasympathetic control, resulting in ... KAch channels activate during hyperpolarization, prolonging the cardiac action potential by inflow of potassium ions and ...
"Challenges in Cardiac Tissue Engineering". Tissue Engineering Part B: Reviews 16 (2): 169-187. doi:10.1089/ten.teb.2009.0352. ... myocytes, marrow adipocytes and beta-pancreatic islets cells. ...
Primary type Ia sensory fibers (large diameter) spiral around all intrafusal muscle fibres, ending near the middle of each fibre. Secondary type II sensory fibers (medium diameter) end adjacent to the central regions of the static bag and chain fibres.[2] These fibres send information by stretch-sensitive mechanically-gated ion-channels of the axons.[3] The motor part of the spindle is provided by motor neurons: up to a dozen gamma motor neurons and one or two beta motor neurons, collectively called fusimotor neurons.[citation needed] These activate the muscle fibres within the spindle. Gamma motor neurons supply only muscle fibres within the spindle, whereas beta motor neurons supply muscle fibres both within and outside of the spindle. Activation of the neurons causes a contraction and stiffening of the end parts of the muscle spindle muscle fibers. Fusimotor neurons are classified as static or dynamic according to the type of muscle fibers they innervate and their effects on the responses of ...
হৃৎপেশী (Cardiac muscle). *অনৈচ্ছিক পেশী (Involuntary muscle). *ঐচ্ছিক পেশী (অস্থিপেশী) (Voluntary/Skeletal muscle) ... পেশীকোষ (Myocyte). *পেশীতন্তু (Myofibril). *পেশী একক (Sarcomere). *মধ্যচ্ছদা (Diaphragm). *উরোস্থি-জক্রক-কর্ণমূল পেশী ( ...
... cardiac myocytes, adipose tissue, fibroblasts, and neurons.[5] Large amounts of TNF are released in response to ...
Cardiac muscle fibers are interconnected by intercalated discs,[12] giving that tissue the appearance of a syncytium. ... The threadlike muscle fibers are the individual muscle cells (myocytes), and each cell is encased within its own endomysium of ... Cardiac muscle (myocardium), is also an "involuntary muscle" but is more akin in structure to skeletal muscle, and is found ... Cardiac and skeletal muscles are "striated" in that they contain sarcomeres that are packed into highly regular arrangements of ...
Because of serotonin's growth-promoting effect on cardiac myocytes,[14] a serotonin-secreting carcinoid tumour may cause a ... It is estimated that less than 6% of carcinoid patients will develop carcinoid syndrome, and of these, 50% will have cardiac ... tricuspid valve disease syndrome, due to the proliferation of myocytes onto the valve.[citation needed] ...
... is a sheath of connective tissue that groups muscle fibers into bundles (anywhere between 10 and 100 or more) or fascicles. Studies of muscle physiology suggest that the perimysium plays a role in transmitting lateral contractile movements. This hypothesis is strongly supported in one exhibition of the existence of "perimysial junctional plates" in ungulate flexor carpi radialis muscles constructed by Emilie Passerieux.[1] The overall comprehensive organization of the perimysium collagen network, as well as its continuity and disparateness, however, have still not been observed and described thoroughly everywhere within the muscle. Found to have type I, III, VI, and XII collagen. ...
Types of muscle are striated muscle (such as skeletal muscle and cardiac muscle), obliquely striated muscle (found in some ... such as skeletal and cardiac muscle, the actin and myosin filaments each have a specific and constant length in the order of a ...
Heart: systolic and diastolic heart failure, likely due to chemical signals that depress myocyte function, cellular damage, ... higher cardiac output, and disorders in blood-clotting that may lead to organ failure.[18] Fever is the most common presenting ... Dobutamine can also be used in hypotensive septic shock to increase cardiac output and correct blood flow to the tissues.[67] ... reducing cardiac contractility and causing heart failure. In the gastrointestinal tract, increased permeability of the mucosa ...
Myocyte *Skeletal striated muscle → 골격근 (D). 신경계통, 18. *Nervous system → 신경계통 (C) ... Cardiac arrest → 심정지 (E). *Hypoxia (medical) → 저산소증 (D). *Inflammation → 염증 (A). *Myocardial infarction → 심근 경색 (B) ...
Findings of the study indicate that diabetes leads to premature myocyte senescence and death and together they result in the ... "Diabetes Promotes Cardiac Stem Cell Aging and Heart Failure, Which Are Prevented by Deletion of the p66shc Gene". Circ. Res. 99 ...
Atrial-natriuretic peptide (ANP) Cardiac myocytes. *Brain natriuretic peptide (BNP) Cardiac myocytes ...
Caveolin-3 Association and Rapid Actions of Vitamin D Receptor in Cardiac Myocytes". Steroids 75 (8-9): 555-9. PMC 2885558. ...
Cardiac action potentialsEdit. Main articles: Cardiac action potential, Electrical conduction system of the heart, Cardiac ... If action potentials in Xenopus myocytes are blocked, the typical increase in sodium and potassium current density is prevented ... The cardiac action potential plays an important role in coordinating the contraction of the heart.[ai] The cardiac cells of the ... In cardiac muscle cells, on the other hand, an initial fast sodium spike provides a "primer" to provoke the rapid onset of a ...
The electrical depolarizations that trigger cardiac myocytes to contract arise spontaneously within the myocyte itself. The ... The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. ... They innervate the heart via sympathetic cardiac nerves that increase cardiac activity and vagus (parasympathetic) nerves that ... Since HRmax varies by individual, the most accurate way of measuring any single person's HRmax is via a cardiac stress test. In ...
Based on different cardiac hypertrophy models, it has been demonstrated that cardiac stress can result in gene expression ... For HDACs 4, 5 and 7, conserved binding domains have been discovered that bind for C-terminal binding protein (CtBP), myocyte ... HDAC9 KO mice are shown to suffer from cardiac hypertrophy which is exacerbated in mice that are double KO for HDACs 9 and 5.[6 ... Studies on p300 and CREB-binding protein linked cardiac hypertrophy with cellular HAT activity suggesting an essential role of ...
"Ablation of nonmuscle myosin II-B and II-C reveals a role for nonmuscle myosin II in cardiac myocyte karyokinesis". Molecular ... myocardial cells contain only NM IIB but NM IIA is more abundant in the non-myocyte cells. NM IIB is predominant in most parts ...
... s are skeletal muscle fibers that serve as specialized sensory organs (proprioceptors) that detect the amount and rate of change in length of a muscle.[1] They constitute the muscle spindle and are innervated by both sensory (afferent) and motor (efferent) fibers. Gamma efferents from small multipolar cells from anterior gray column innervate it. These form a part of neuromuscular spindles. Intrafusal muscle fibers are walled off from the rest of the muscle by an outer connective tissue sheath consisting of flattened fibroblasts and collagen.[2] This sheath has a spindle or "fusiform" shape, hence the name "intrafusal". There are two types of intrafusal muscle fibers: nuclear bag and nuclear chain fibers. They bear two types of sensory ending, known as annulospiral and flower-spray endings. Both ends of these fibers contract but the central region only stretches and does not contract. They are innervated by gamma motor neurons and beta motor neurons. It is by the sensory ...
myocyte (cardiac muscle). cardiovascular. *norepinephrine → β-adrenergic receptor. *sequester Ca2+ in sarcoplasmic reticulum * ... myocyte (skeletal muscle). muscular system. *epinephrine → β-adrenergic receptor. *produce glucose *stimulate glycogenolysis * ... In cardiac muscleEdit. In a cascade mediated by a GPCR known as β1 adrenoceptor, activated by catecholamines (notably ... myocyte (smooth muscle). cardiovascular. *β2 adrenergic agonists → β-2 adrenergic receptor. *histamine → Histamine H2 receptor ...
"Evidence that human cardiac myocytes divide after myocardial infarction". The New England Journal of Medicine. 344 (23): 1750-7 ... Cardiac myocyte renewal has been found to occur in normal adult humans,[94] and at a higher rate in adults following acute ... of myocytes around the area of injury, which is not enough to restore function of cardiac muscle. However, this may be an ... MRL mice show the same amount of cardiac injury and scar formation as normal mice after a heart attack.[84] However, recent ...
Heart: systolic and diastolic heart failure, likely due to chemical signals that depress myocyte function, cellular damage, ... Other measurements such as cardiac output and superior vena cava oxygen saturation may be used.[4] People with sepsis need ... higher cardiac output, and disorders in blood-clotting that may lead to organ failure.[15] ... Dobutamine can also be used in hypotensive septic shock to increase cardiac output and correct blood flow to the tissues.[61] ...
In cardiac myocytes this forms a scalloped surface.[10]. The cytoskeleton is what the rest of the cell builds off of and has ... A myocyte (also known as a muscle cell)[1] is the type of cell found in muscle tissue. Myocytes are long, tubular cells that ... Individual myocytes are surrounded by endomysium. Myocytes are bound together by perimysium into bundles called fascicles; the ... This contraction of the myocyte is triggered by the action potential over the cell membrane of the myocyte. The action ...
Non-cardiac manifestations[19]. Upper limb abnormalities. Small or absent thymus Small or absent parathyroids Facial ... myocytes) around it by day 21. On day 22, the heart begins to beat and by day 24, blood is circulating.[26] ... A number of genes have been associated with cardiac manifestations. Mutations of a heart muscle protein, α-myosin heavy chain ( ... Niessen, K.; Karsan, A. (2008). "Notch Signaling in Cardiac Development". Circulation Research. 102 (10): 1169-1181. doi: ...
Muscle cells (myocytes) form the active contractile tissue of the body. Muscle tissue functions to produce force and cause ... Cardiac muscle is found only in the heart, allowing it to contract and pump blood round the body. ... Muscle is formed of contractile filaments and is separated into three main types; smooth muscle, skeletal muscle and cardiac ...
The cardiac conduction system (and AV node part of it) coordinates myocyte mechanical activity. A wave of excitation spreads ... The atrioventricular node delays impulses by approximately 0.09s. This delay in the cardiac pulse is extremely important: It ... BMP (Bone morphogenetic protein) cell signaling plays a key role in diverse aspects of cardiac differentiation and ... Journal of Interventional Cardiac Electrophysiology. 7 (2): 137-48. doi:10.1023/A:1020833604423. PMID 12397223. Guyton, Arthur ...
Studies conducted on cultured myocytes, a form of muscle cell, indicates that LECT2 impairs insulin signaling by activating a c ... Several cell types or tissues, e.g. osteoblasts, chondrocytes, cardiac tissue, gastrointestinal smooth muscle cells, and ...
Chief among these are modulation of Ca2+ release, modulation of cardiac myocyte contractility, and inhibition of voltage gated ...
Heart-type Fatty Acid-Binding Protein (H-FABP) is a small cytoplasmic protein (15 kDa) released from cardiac myocytes following ... "Cloning and characterization of a novel cardiac-specific kinase that interacts specifically with cardiac troponin I". Journal ... "Cloning and characterization of a novel cardiac-specific kinase that interacts specifically with cardiac troponin I". Journal ... FABP3 is known to interact with TNNI3K in the context of interacting with cardiac troponin I. The protein also interacts with, ...
Myocytes, Cardiac. Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC). ... All MeSH CategoriesAnatomy CategoryCardiovascular SystemHeartMyocardiumMyocytes, Cardiac. All MeSH CategoriesAnatomy Category ... TissuesMusclesMuscle, StriatedMyocardiumMyocytes, Cardiac. All MeSH CategoriesAnatomy CategoryCellsMuscle CellsMyocytes, ...
Cardiac Myocytes flies the cardiac progenitor cells (CPCs) in a Techshot Bioreactor on the ISS and evaluates myocyte maturation ... Conversion of Adipogenic Mesenchymal Stem Cells into Mature Cardiac Myocytes (Cardiac Myocytes) - 09.27.17. Overview , ... Ground studies for Conversion of Adipogenic Mesenchymal Stem Cells into Mature Cardiac Myocytes (Cardiac Myocytes) are complete ... Conversion of Adipogenic Mesenchymal Stem Cells into Mature Cardiac Myocytes (Cardiac Myocytes) uses the microgravity ...
Seminar by Professor Angela Clerk on Signalling to gene expression in cardiac myocytes. ... Signalling to gene expression in cardiac myocytes. Abstract. Cardiomyocytes, the terminally-differentiated contractile cells ...
An automated method measuring cardiac myocyte surface area was described and used as an index of cell growth. Hearts from 2 to ... An automated method measuring cardiac myocyte surface area was described and used as an index of cell growth. Hearts from 2 to ... Areas of individual myocytes varied widely, with the distribution skewed toward larger cells. The standard deviation increased ...
Calcium homeostasis in cardiac myocytes results from the integrated function of transsarcolemmal Ca2+ influx and efflux ... It may be anticipated that a rapid increase in our understanding of the pathophysiology of Ca2+ homeostasis in cardiac myocytes ... Intracellular calcium homeostasis in cardiac myocytes.. W H Barry, J H Bridge ...
Furthermore, dysfunction of calcium dynamics also is thought to play a role in cardiac arrhythmias. A combination of ... Furthermore, dysfunction of calcium dynamics also is thought to play a role in cardiac arrhythmias. A combination of ...
... three decades of pharmacological data have clearly implicated PDE3 in cardiac function. Conversely, much less was known about ... McCahill A, Campbell L, McSorley T, Sood A, Lynch MJ, Li X, Yan C, Baillie GS, Houslay MD (2008a) In cardiac myocytes, cAMP ... In this chapter, the molecular properties and function of PDE4s in the different compartments of the cardiac myocytes will be ... Bers DM (2008) Calcium cycling and signaling in cardiac myocytes. Annu Rev Physiol 70:23-49. doi: 10.1146/annurev.physiol. ...
In cardiac myocytes, the AP upstroke triggers nearly synchronized Ca2+ release, causing RyRs to recover and hence SCR to occur ... 2007) Analysis of ryanodine receptor clusters in rat and human cardiac myocytes. Proc Natl Acad Sci USA 104(38):14958-14963. ... 2011) A mathematical model of spontaneous calcium release in cardiac myocytes. Am J Physiol Heart Circ Physiol 300(5):H1794- ... Cardiac myocytes normally initiate action potentials in response to a current stimulus that depolarizes the membrane above an ...
... a computational framework for the comprehensive assessment of contractile responses of enzymatically dissociated adult cardiac ... myocytes. The proposed methodology comprises the following stages: digital video recording of the contracting cell, edge ... atrial myocytes and isolated smooth muscle cells, or in cardiac myocytes which develop spatially nonuniform oscillatory ... The cardiac myocyte is approximately 25 m in diameter and about 100 m in length. It is composed of bundles of myofibrils that ...
... molecular composition and electrophysiological properties of cardiac myocytes and functional characteristics of the fish heart ... Plasticity of excitation-contraction coupling in fish cardiac myocytes Comp Biochem Physiol A Mol Integr Physiol. 2002 Aug;132( ... Consequently excitation-contraction coupling of the fish cardiac myocytes is not a fixed entity, but rather a highly variable ... Ultrastructure, molecular composition and electrophysiological properties of cardiac myocytes and functional characteristics of ...
Effects of cholesterol depletion on compartmentalized cAMP responses in adult cardiac myocytes.. Agarwal SR1, MacDougall DA, ... Effects of cholesterol depletion on compartmentalized cAMP responses in adult cardiac myocytes ... Effects of cholesterol depletion on compartmentalized cAMP responses in adult cardiac myocytes ... Effects of cholesterol depletion on compartmentalized cAMP responses in adult cardiac myocytes ...
Cardiac Troponins are specific to the cardiac myocyte and have central role in diagnosing ACS. They are found to be specific ... Cardiac Troponins are specific to the cardiac myocyte and have central role in diagnosing ACS. They are found to be specific ... More about Cardiac Troponins And The Cardiac Myocyte. *. The Heart Of Myocardial Infraction. 1165 Words , 5 Pages ... 6 How does the structure of cardiac myocytes and intercalated disks follow the function of cardiac muscle tissue and the ...
Gene context of Myocytes, Cardiac. *TGF-beta reduced expression of cardiac myocyte iNOS message and protein, reduced nitrite ... Disease relevance of Myocytes, Cardiac. *Thus, cardiac myocyte apoptosis is a critical point in the transition between ... on cardiac myocyte cytotoxicity, we exposed adult rat cardiac myocytes to either cytokines alone or to activated J774 ... To test the hypothesis that cytokines can modulate cardiac myocyte growth and phenotype, myocytes cultured from neonatal rat ...
... in cardiac myocyte medium (CMM) supplemented with 5% FBS, 1% cardiac myocyte growth supplement, and 1% penicillin/streptomycin ... Antiapoptotic Actions of Methyl Gallate on Neonatal Rat Cardiac Myocytes Exposed to H2O2. Sandhya Khurana,1 Amanda ... S. A. Cook and P. A. Poole-Wilson, "Cardiac myocyte apoptosis," European Heart Journal, vol. 20, no. 22, pp. 1619-1629, 1999. ... M. T. Crow, K. Mani, Y.-J. Nam, and R. N. Kitsis, "The mitochondrial death pathway and cardiac myocyte apoptosis," Circulation ...
The thromboxane A2 mimic U46619 increases calcium transients in rat cardiac myocytes.. ... in isolated cardiac myocytes from neonatal rats. The TXA2 mimic U46619 (0.1 - 1 microM) markedly increased the height and width ...
... involved in mediating cardiac myocyte hypertrophy, and has enabled the molecular dissection of the pathways involved in signal ... Previous Document: Phosphatidic acid: a potential signal transducer for cardiac hypertrophy.. Next Document: Molecular ... mechanisms of angiotensin II in modulating cardiac function: intracardiac effects and sign.... ...
Free, long-chain, polyunsaturated fatty acids reduce membrane electrical excitability in neonatal rat cardiac myocytes.. J X ... Free, long-chain, polyunsaturated fatty acids reduce membrane electrical excitability in neonatal rat cardiac myocytes. ... Free, long-chain, polyunsaturated fatty acids reduce membrane electrical excitability in neonatal rat cardiac myocytes. ... Free, long-chain, polyunsaturated fatty acids reduce membrane electrical excitability in neonatal rat cardiac myocytes. ...
Light micrograph of cardiac myocytes stained with a specific method for lipofuscin (Long Ziehl-Neelsen). The lipofuscin ... Light micrograph of cardiac myocytes stained with a specific method for lipofuscin (Long Ziehl-Neelsen). The lipofuscin ...
... Am J Physiol Heart Circ Physiol. 2007 Jun;292(6): ... as is whether it is released by cardiac myocytes. We investigated several different pathways controlling protein release ...
Isolation of cardiac myocytes histidyl dipeptide treatment. Cardiac myocytes were isolated from adult C57/BL6 mice by using a ... Pretreatment of cardiac myocytes with carnosine increased the mean lifetime of myocytes superfused with HNE or acrolein ... As before, adult cardiac myocytes were pretreated with 1 mM each of carnosine, DMB and balenine for 12-16 h and then superfused ... To ensure that the dipeptides are taken up by the cardiac myocytes, we incubated these cells with 1 mM of each carnosine, ...
Haloperidol Prolongs Diastolic Phase of Ca^,2+, Transient in Cardiac Myocytes * * Ishida Hideyuki ISHIDA Hideyuki ... Kinetics of chlorpromazine block of sodium channels in single guinea pig cardiac myocytes OGATA N. ... transient and on cell motion in cultured cardiac myocytes, as well as the pathways involving the HPL-induced abnormality of Ca, ... Effects of overexpression of the Na^+-Ca^,2+, exchanger on [Ca^,2+,]_i transients in murine ventricular myocytes YAO A. ...
Abstract 846: Chronic Cardiac Resynchronization Reverses Abnormal Calcium Handling in Failing Ventricular Myocytes. Serge ... Abstract 846: Chronic Cardiac Resynchronization Reverses Abnormal Calcium Handling in Failing Ventricular Myocytes ... Abstract 846: Chronic Cardiac Resynchronization Reverses Abnormal Calcium Handling in Failing Ventricular Myocytes ... Abstract 846: Chronic Cardiac Resynchronization Reverses Abnormal Calcium Handling in Failing Ventricular Myocytes ...
In cardiac myocytes, NAADP is thought to stimulate calcium release from acidic stores which then bolsters filling and release ... Basal cardiac rate is a major determinant in cardiac mortality and compounds which specifically affect rate have clinical ... Modulation of cardiac rate and contraction through calcium-dependent and independent means are of central import to the ability ... In contractile myocytes, photorelease of NAADP caused significant increase in calcium transient amplitude and velocity of ...
Understanding the molecular mechanisms that regulate the proliferation and differentiation of cardiac myocytes will ai ... We propose that embryonic cardiac myocytes grown on the tube substrate develop into neonatal cardiac myocytes via normal in ... In addition, embryonic cardiac myocytes grown on the tubular substrate have an aligned phenotype that closely resembles in vivo ... Here we report the development of a model system that recapitulates many aspects of cardiac myocyte differentiation that occur ...
Human Cardiac Myocytes (HCM). Primary Human Cardiac Myocytes isolated from the ventricles of the adult heart. ... Primary Human Cardiac Myocytes (HCM) are isolated from the ventricles of the adult heart. They are qualified for in vitro ... Figure 1. Human Cardiac Muscle Cell Culture in phase contrast. Figure 1. Human Cardiac Muscle Cell Culture in phase contrast. ... research on cardiac diseases and for pharmacological studies. Unlike freshly isolated rod-shaped myocytes, cultured HCM can be ...
No significant cytotoxic or apoptotic effects were observed on fetal cardiac myocytes after 24 and 48 hours of exposure with ... No significant cytotoxic or apoptotic effects were observed on fetal cardiac myocytes after 24 and 48 hours of exposure with ... we demonstrate for the first time that the designed NPs can be used as potential probes for drug delivery in cardiac myocytes. ... we demonstrate for the first time that the designed NPs can be used as potential probes for drug delivery in cardiac myocytes. ...
Bipin G. Nair, and Tarun B Patel, "Epidermal growth factor stimulates cAMP accumulation in cultured rat cardiac myocytes", ... studies presented here was to determine whether or not the effects of EGF on adenylyl cyclase were mediated in cardiac myocytes ... We have previously shown that epidermal growth factor (EGF) augments cAMP accumulation in the heart and stimulates cardiac ... we have demonstrated that Gs alpha mediates the effects of EGF on cardiac adenylyl cyclase (Nair et al., 1990). Since the heart ...
Ang II-induced translocation of RhoA from the soluble to the particulate fractions in cardiac myocytes. A, Cardiac myocytes ... In vivo ADP-ribosylation of Rho in cardiac myocytes. Cardiac myocytes were incubated with the indicated concentrations of C3 ... Colocalization of polymerized actin and troponin T in cardiac myocytes. Cardiac myocytes stimulated with Ang II for 30 minutes ... Ang II-induced sarcomeric actin organization in cardiac myocytes. Cardiac myocytes grown on gelatin-coated glass coverslips ...
Atrial myocytes demonstrate the diversity of cardiac calcium signalling.. Channels, 9(5) pp. 219-220. ...
Cardiac myocyte explanation free. What is Cardiac myocyte? Meaning of Cardiac myocyte medical term. What does Cardiac myocyte ... Looking for online definition of Cardiac myocyte in the Medical Dictionary? ... redirected from Cardiac myocyte). Also found in: Dictionary, Thesaurus, Encyclopedia.. Related to Cardiac myocyte: cardiac ... Cardiac myocyte , definition of Cardiac myocyte by Medical dictionary ...
  • Recent studies have demonstrated inducible NO production within the heart, and that cytokine-induced NO mediates alterations in cardiac contractility, but the cytotoxic potential of nitric oxide with respect to the heart has not been defined. (
  • Reduced cardiac contractility during heart failure (HF) is linked to impaired Ca 2+ release from Ryanodine Receptors (RyRs). (
  • It is concluded (1) that the density of sarcolemmal Ca2+ current is not increased after acclimation to cold, (2) that sarcolemmal Ca2+ influx through L-type Ca2+ channels can make a significant contribution to contractile [Ca2+] in both teleost species studied and (3) that ss-adrenergic stimulation of Ca2+ current is more important in modulating cardiac contractility in trout than in carp. (
  • But their success appears counterintuitive because they block the β1-adrenergic signaling pathway in cardiac myocytes, which enhances cardiac contractility. (
  • This has led to the suggestion that downregulation of Na + -K + -ATPase in the failing heart may be an adaptive response leading to increased contractility by a mechanism similar to that induced by cardiac glycosides ( 8 , 21 , 28 ). (
  • Methods and Results- We analyzed contractility in the whole rat heart, adult rat ventricular myocytes (ARVMs), and myofibrils from both sexes of rats and observed functional sex differences at all levels. (
  • Aims Glucocorticoid (GC) stimulation has been shown to increase cardiac contractility by elevated intracellular [Ca] but the sources for Ca entry are unclear. (
  • Short-term GC-stimulation with Dex improves cardiac contractility by a SOCE-dependent mechanism, which appears to involve increased SGK1-dependent expression of the SOCE-related proteins. (
  • Both IL-1β and SNP significantly elevated maximum diastolic potential, reduced peak calcium current (I Ca ), and lowered contractility in the myocytes. (
  • These data suggest that IL-1β-induced NO production in cardiac myocytes lowers energy production and myocardial contractility through a direct attack on the mitochondria, rather than through cGMP-mediated pathways. (
  • The second messenger cyclic adenosine monophosphate (cAMP) is the most important modulator of sympathetic control over cardiac contractility. (
  • Polyphenols like epigallocatechin gallate (EGCG) can reduce apoptosis of cardiomyocytes, resulting in better health outcomes in animal models of cardiac disorders. (
  • Cardiomyocytes also undergo cell death under a variety of other physiological stimuli such as oxidative stress due to hypoxia induced during cardiac ischemia and glucose limitation amongst others [ 11 ]. (
  • The use of cardiomyocytes in cell culture has identified, besides mechanical loading, a range of substances, such as cytokines, growth factors, catecholamines, vasoactive peptides and hormones, involved in mediating cardiac myocyte hypertrophy, and has enabled the molecular dissection of the pathways involved in signal transduction. (
  • Electrophysiological/pharmacological evidence suggests that "neuronal" isoform(s) exist in cardiomyocytes along with the cardiac-dominant NaV1.5. (
  • Strategic localization of IP 3 Rs in cytoplasmic compartments and the nucleus enables them to participate in subsarcolemmal, bulk cytoplasmic and nuclear Ca 2+ signaling in embryonic stem cell-derived and neonatal cardiomyocytes, and in adult cardiac myocytes from the atria and ventricles. (
  • Canine cardiomyocytes were used as a model system to study structural changes in the sarcomere associated cytoskeletal protein, alpha-actinin, after inducing synchronous or dyssynchronous heart failure (SHF or DHF) and following cardiac resynchronization therapy (CRT). (
  • miR-208a was upregulated in cardiomyocytes and cardiomyocyte-derived exosomes from both models of cardiac fibrosis and could be transferred into cardiac fibroblasts via the exosomes. (
  • Cardiomyocytes participate in cardiac fibrosis by secreting exosomes containing miR-208a, which increases fibroblast proliferation and differentiation into myofibroblasts. (
  • The coordinated migration of bilateral cardiomyocytes and the formation of the cardiac cone are essential for heart tube formation. (
  • Importantly, because both hypoxia and oxidant stress prevail in a setting of ischemia and reperfusion, the effects of soluble factors from hypoxic fibroblasts on the MPT-ROS threshold and viability of myocytes may represent a novel paracrine mechanism that could exacerbate ischemia-reperfusion injury to cardiomyocytes. (
  • Introduction Neurogenic stunned myocardium (NSM) is a condition that neurogenic insults lead to transit cardiac dysfunctions, which mimics the clinical presentations of acute coronary syndrome. (
  • We examined how many myocytes and how much myocardium these concentrations represent. (
  • METHODS: Individual rat cardiac myocytes, rat myocar- dium, ovine myocardium, or human myocardium were spiked into 400- L aliquots of human serum. (
  • Using transgenic mice that express a conditionally active caspase exclusively in the myocardium, we demonstrate that very low levels of myocyte apoptosis (23 myocytes per 10 5 nuclei, compared with 1.5 myocytes per 10 5 nuclei in controls) are sufficient to cause a lethal, dilated cardiomyopathy. (
  • These findings on infected cardiac myocytes in culture reveal that alterations in cardiac gene expression described in Chagas disease are the consequence of both direct infection of the myocytes themselves as well as resulting from the presence of other cell types in the myocardium and systemic effects of infection. (
  • During normal contraction, calcium (Ca 2+ ) release from the sarcoplasmic reticulum (SR)-the intracellular Ca 2+ store of a ventricular myocyte-is triggered by Ca 2+ entry into the cell via L-type calcium channels (LCCs), a mechanism known as Ca 2+ -induced Ca 2+ -release (CICR). (
  • The proposed method not only provides a more comprehensive assessment of the myocyte contraction process but also can potentially eliminate historical concerns and sources of errors caused by myocyte rotation or translation during contraction. (
  • Furthermore, the versatility of the image processing techniques makes the method suitable for determining myocyte shortening in cells that usually bend or move during contraction. (
  • Ultrastructure, molecular composition and electrophysiological properties of cardiac myocytes and functional characteristics of the fish heart suggest that cycling of extracellular Ca(2+) is generally more important than intracellular cycling of Ca(2+) stores of the sarcoplasmic reticulum (SR) in activating contraction of fish cardiac myocytes. (
  • However, prominent species-specific differences exist in cardiac excitation-contraction coupling and in the relative roles of extracellular and intracellular Ca(2+) sources among the teleostean fish. (
  • Consequently excitation-contraction coupling of the fish cardiac myocytes is not a fixed entity, but rather a highly variable and malleable process that enables fish to have an appropriate cardiac scope to exploit a diverse range of environments. (
  • Because previous studies showed that polyunsaturated fatty acids can reduce the contraction rate of spontaneously beating heart cells and have antiarrhythmic effects, we examined the effects of the fatty acids on the electrophysiology of the cardiac cycle in isolated neonatal rat cardiac myocytes. (
  • Modulation of cardiac rate and contraction through calcium-dependent and independent means are of central import to the ability of an organism to adapt to its environment. (
  • The action of cardiac fibres is to produce strong and rhythmic contractions from within, even when removed from the body (see MYOGENIC CONTRACTION ). (
  • Type of myocyte that is responsible for heart contraction. (
  • The basic processes for cardiac excitation-contraction coupling are well described. (
  • Cardiac excitation-contraction coupling relies largely on ryanodine receptor (RyR)-induced Ca 2+ release from the sarcoplasmic reticulum. (
  • In the heart, cardiac glycosides increase the force of contraction, the positive inotropic effect that is the basis of the continued use of these drugs in the management of congestive heart failure ( 1 , 32 , 35 ). (
  • Thapsigargin increases cardiac myocyte contraction (7). (
  • Another important ion is calcium (Ca2+), which can be found outside of the cell as well as inside the cell, in a calcium store known as the sarcoplasmic reticulum (SR). Release of Ca2+ from the SR, via a process called calcium-induced calcium release, is vital for the plateau phase of the action potential (see phase 2, below) and is a fundamental step in cardiac excitation-contraction coupling. (
  • Intracellular calcium homeostasis in cardiac myocytes. (
  • Calcium homeostasis in cardiac myocytes results from the integrated function of transsarcolemmal Ca2+ influx and efflux pathways modulated by membrane potential and from intracellular Ca2+ uptake and release caused predominantly by SR function. (
  • Recent reports indicate that TXA2 induced platelet aggregation is associated with an increase in cytosolic Ca. The present study was designed to determine if TXA2 had a comparable effect on intracellular Ca transients (measured with fura-2) in isolated cardiac myocytes from neonatal rats. (
  • The aim of the studentship is to characterise and produce a model of the cardiac myocyte action potential to study the electrical properties of the heart through applying existing techniques (e.g. sharp intracellular recordings, computational modelling) as well as the development of new techniques (e.g. whole-cell patch). (
  • The partial inhibition of the cardiac myocyte Na + -K + -ATPase that produces a modest increase in intracellular Na + concentration ([Na + ] i ) is sufficient to affect the sarcolemmal Na + /Ca 2+ exchanger to cause significant increases in intracellular Ca 2+ concentration ([Ca 2+ ] i ) and in the contractile force ( 1 , 32 ). (
  • This resulted in a steady increase in intracellular ROS in cultured cardiac myocytes for at least 12 h. (
  • Intracellular reactive oxygen species mediate the linkage of Na+/K+-ATPase to hypertrophy and its marker genes in cardiac myocytes. (
  • Furthermore, dysfunction of calcium dynamics also is thought to play a role in cardiac arrhythmias. (
  • Our results establish a theoretical framework for interpreting complex and varied manifestations of triggered activity relevant to cardiac arrhythmias. (
  • Death due to ischemic heart disease (IHD) is the result of cardiac arrhythmias and loss of cardiac pump function. (
  • The antimuscarinic effect of cocaine may play an important role in cocaine cardiotoxicity by reducing the membrane electrical stability and acting synergistically with other actions of cocaine to facilitate the occurrence of lethal cardiac arrhythmias. (
  • Cocaine use poses a major health problem not only because of the dependence it causes but also because of the generation of life-threatening cardiac arrhythmias following overdose. (
  • Additionally, modulation of electrical activity of cardiac myocyte by natural occurring chemical compounds may present a therapeutic application, especially in the context of cardiac arrhythmias (Li et al. (
  • We investigated whether signaling events mediated by the RhoA/Rho-associated coiled coil-containing kinase (ROCK) pathway are involved in regulation of stretch-induced FAK phosphorylation at Tyr 397 in neonatal rat ventricular myocytes (NRVMs). (
  • On the other hand, FAK activation in neonatal rat ventricular myocytes (NRVMs) by agonists such as endothelin has been demonstrated ( 16 ) to be dependent on activation of the RhoA/Rho-associated coiled coil-containing protein kinase (ROCK) signaling pathway, which drives the assembly and rearrangement of actin filaments. (
  • In neonatal rat ventricular myocytes (NVRM), knockdown of HKI, but not HKII, decreased glycolytic activity. (
  • Cardiac fibrosis is primarily mediated by activated fibroblasts. (
  • Structural and functional coupling of cardiac myocytes and fibroblasts. (
  • Cardiac myocytes and fibroblasts form extensive networks in the heart, with numerous anatomical contacts between cells. (
  • The myocyte network, coupled by gap junctions, is generally believed to be electrically isolated from fibroblasts in vivo. (
  • In culture, however, the heterogeneous cell types form functional gap junctions, which can provide a substrate for electrical coupling of distant myocytes, interconnected by fibroblasts only. (
  • Zhang X, Azhar G, Nagano K, Wei JY (2001) Differential vulnerability to oxidative stress in rat cardiac myocytes versus fibroblasts. (
  • Cardiac fibroblasts contribute to multiple aspects of myocardial function and pathophysiology. (
  • With the use of an in vitro cell culture model, this study evaluated cytokine production by hypoxic cardiac fibroblasts and examined two distinct effects of hypoxic fibroblast-conditioned medium (HFCM) on cardiac myocytes and fibroblasts. (
  • Hypoxia caused a marked increase in the production of tumor necrosis factor (TNF)-α by cardiac fibroblasts. (
  • HFCM also decreased DNA synthesis in cardiac fibroblasts. (
  • Normoxic fibroblast-conditioned medium spiked with TNF-α at 200 pg/ml, a concentration comparable to that in HFCM, promoted loss of myocyte viability and decreased DNA synthesis in cardiac fibroblasts. (
  • A specialized population of Periostin-expressing cardiac fibroblasts contributes to postnatal cardiomyocyte maturation and innervation. (
  • Ultimately, understanding how the highly interactive mechanical signaling can give rise to phenotypic changes is critical for targeting the underlying pathways that contribute to cardiac remodeling associated with various forms of dilated and hypertrophic myopathies, myocardial infarction, heart failure, and reverse remodeling. (
  • the activation of oxidative stress pathways in utero can program for cardiac dysfunction in adulthood such as responses to ischemia/reperfusion, cardiac function, coronary flow, and hypertension [ 4 - 7 ]. (
  • Signaling pathways in cardiac myocyte hypertrophy. (
  • Numerous signal transduction pathways have been shown to be activated in cardiac myocytes subjected to mechanical stimuli ( 35 ). (
  • Signals originating from multiple pathways converge intracellularly, leading to altered gene expression and protein synthesis, which result in the hypertrophic growth of cardiac myocytes. (
  • Several lines of evidence support a role for FAK in the regulation of early gene transcription in response to hypertrophic agonists and mechanical stress ( 10 , 22 , 28 , 38 , 39 ), indicating that this kinase may coordinate the convergence of multiple signaling pathways involved in the hypertrophic growth of cardiac myocytes. (
  • These data demonstrate that MSK1 activation in adult rat cardiac myocytes by G-protein-coupled receptor agonists requires the simultaneous activation of both the ERK and p38 MAPK pathways. (
  • A major goal in this area has been to identify the mechanisms that link biomechanical forces to the activation of signaling pathways that mediate the hypertrophic as well as maladaptive responses of cardiac myocytes to mechanical stress. (
  • Redox sensitive signaling pathways in cardiac remodeling, hypertrophy and failure. (
  • Highly specific and potent kinase inhibitors developed by Cytopia have been shown to block signaling pathways in cardiac myocytes that are associated with heart failure. (
  • Cardiac and vascular cell death by apoptosis is not only a feature of embryologic and neonatal development, but can be elicited by a variety of diverse stimuli (Table I) and has been linked to virtually every major cardiovascular disease or disorder (Table II). (
  • In this experimental model, increased cardiac myocyte apoptosis (Figure 1C) can be linked to the reduction in myocyte fractional mass (Figure 1A) as the hearts progress to failure. (
  • Long X, Boluyt MO, Zheng JS, O'Neill L, Pirelli C, Lakatta EG, Crow MT. p53 and the hypoxia-induced apoptosis of cultured neonatal rat cardiac myocytes. (
  • Exposure of isolated cardiac myocytes to chronic hypoxia followed by reoxygenation results in the early activation of c-Jun N-terminal kinase (JNK) and death by apoptosis of approx. (
  • Recent studies have identified low levels of myocyte apoptosis (80-250 myocytes per 10 5 nuclei) in failing human hearts. (
  • To our knowledge, these data provide the first direct evidence that myocyte apoptosis may be a causal mechanism of heart failure, and they suggest that inhibition of this cell death process may constitute the basis for novel therapies. (
  • Abstract -The organization of actin into striated fibers (myofibrils) is one of the major features of cardiac hypertrophy. (
  • Abstract -Although the cationic inward rectifiers (Kir and hyperpolarization-activated I f channels) have been well characterized in cardiac myocytes, the expression and physiological role of anionic inward rectifiers in heart are unknown. (
  • Oxidative stress has been clinically shown to be relevant in the progression of cardiac diseases and heart failure [ 1 , 2 ]. (
  • They are qualified for in vitro research on cardiac diseases and for pharmacological studies. (
  • Human induced pluripotent stem cells (iPSCs) represent a powerful human model to study cardiac disease in vitro, notably channelopathies and sarcomeric cardiomyopathies. (
  • This hypothesis is supported by in vitro studies, in which cardiac myocytes cultured on collagen or laminin-coated deformable membranes, display hypertrophic responses when exposed to mechanical stretch [ 4 ]. (
  • Prostaglandin F2 alpha induces cardiac myocyte hypertrophy in vitro and cardiac growth in vivo. (
  • Using a different approach, here we report studies on cultured rat neonatal cardiac myocytes showing that Na + -K + - ATPase function is impaired by the overexpression of a fragment of one of its subunits, and we compare some functional consequences of this downregulation with those of the ouabain-induced inhibition of the enzyme. (
  • Conclusion: Platelet gel is cardioprotective to non- ischemic reperfused cardiac tissue after acute myocardial infarction and reperfusion. (
  • Cardiovascular diseases such as hypertension and myocardial infarction are often associated with the development of cardiac hypertrophy. (
  • The amount of PGF2 alpha extractable from the hearts of rats with cardiac hypertrophy induced by myocardial infarction was also found to be greater than that in sham -operated control rats. (
  • When miR-208a was inhibited in vivo, cardiac function improved and cardiac fibrosis was alleviated in post-myocardial-infarction rats. (
  • BACKGROUND: Myocardial infarction is diagnosed when biomarkers of cardiac necrosis exceed the 99th centile, although guidelines advocate even lower concentrations for early rule-out. (
  • 2001), where they may produce direct effects on cardiac myocytes , resulting in inflammation, arrhythmia, or myocardial infarction. (
  • 3) Define the contribution of Abcg2-positive cells to cardiac myocyte creation after myocardial infarction, using fate mapping techniques with tamoxifen-dependent Cre recombinase driven by the Abcg2 locus. (
  • Understanding the molecular mechanisms that regulate the proliferation and differentiation of cardiac myocytes will aid in designing therapies for myocardial repair. (
  • Here we report the development of a model system that recapitulates many aspects of cardiac myocyte differentiation that occur during early cardiac development. (
  • This model will aid in the elucidation of the molecular mechanisms that regulate cardiac myocyte proliferation and differentiation, which will provide important insights into myocardial development. (
  • Different protocols for cardiac differentiation of iPSCs have been proposed either based on embroid body formation (3D) or, more recently, on monolayer culture (2D). (
  • Differentiation of cardiac myocytes with 2D monolayer-based protocols and the use of IWP2 allows the production of higher yield of cardiac myocytes that have more suitable characteristics to study sarcomeric cardiomyopathies. (
  • Conversion of Adipogenic Mesenchymal Stem Cells into Mature Cardiac Myocytes (Cardiac Myocytes) uses the microgravity environment of space to examine how stem cells differentiate into specialized heart cells (cardiac myocytes). (
  • The Cardiac Myocytes experiment delivers frozen stem cells in an experimental setup to the International Space Station where the cells are thawed, cultured under specific conditions, tagged and then returned to Earth for analysis and comparison with control batches. (
  • Ground studies for Conversion of Adipogenic Mesenchymal Stem Cells into Mature Cardiac Myocytes (Cardiac Myocytes) are complete and found that a pair of human transcription factors, ETS2 and MESP1, converted human fat stem cell into cardiac myocytes that were immature. (
  • The experimental paradigm contributes to a novel regenerative strategy that enhanced myocyte maturation occurred from converted human fat stem cells. (
  • Cardiac Myocytes flies the cardiac progenitor cells (CPCs) in a Techshot Bioreactor on the ISS and evaluates myocyte maturation under microgravity conditions. (
  • Thus, research sponsored by the center for the Advancement of Science in Space (CASIS) supports the first conversion of human adipose-derived mesenchymal stem cells (ADMSCs) into cardiac myocytes. (
  • The human adult adipogenic (fat) mesenchymal stem cells (hADMSCs) are reprogrammed to form cardiac progenitors (CPCs) in bulk culture and are infected in the Schwartz laboratory to carry a myosin light chain 2V-Green fluorescent reporter and a luciferase constitutive vector to produce light emissions, important for following reprogrammed cells injected into infarcted hearts. (
  • Areas of individual myocytes varied widely, with the distribution skewed toward larger cells. (
  • To date, at least seven different PDE4 proteins encoded in the four PDE4 genes have been detected in cardiac cells. (
  • Our results provide mechanistic insights into cardiac arrhythmogenesis and highlight important differences between Ca 2+ dynamics in cardiac myocytes and other eukaryotic cells. (
  • We feature the design and application of engineered cellular microenvironments to demonstrate the ability of cardiac cells to remodel their cytoskeletal organization and shape, including sarcomere/myofibrillar architectural topography. (
  • For the cardiac muscle cells to contract, the levels of calcium ions in the cells needs to rapidly increase. (
  • Calcium ions are released in cardiac muscle cells through protein channels called ryanodine receptors. (
  • Further experiments showed that calcium ions 'leak' from these smaller clusters, reducing the amount of calcium that can be released into cardiac muscle cells during each heartbeat. (
  • Maximal beta-adrenergic stimulation increased Ca2+ current by approximately 2.3-fold in trout but by only 1.4-fold in crucian carp, so that Ca2+ current densities in the presence of 10 micromol l-1 isoprenaline were almost equal in trout (8.6-10.5 pA pF-1) and carp (9.6-10.4 pA pF-1) cardiac cells. (
  • In trout cardiac cells, thermal acclimation had no effects on the density of Ca2+ current, but the rate of current inactivation was accelerated after acclimation to cold temperature. (
  • Recent developments in this field indicate that the integrity of structures such as the Z disk, costamere, and intercalated disk is critically important to the ability of cardiac cells to appropriately respond to mechanical stress ( 4 , 11 , 21 , 32 , 37 , 41 ). (
  • The density of I K(ACh) is almost 5 times greater in atrial cells than in left ventricular myocytes. (
  • We have used microarray analysis and siRNA directed against the cardiac-specific transcription factor Nkx2.5 and one of its targets Cripto in P19 clone 6 (P19Cl6) cells to identify potential targets for these genes. (
  • Cultured rat cardiac myocytes and A7r5 cells were transfected with an adenoviral vector used earlier for in vivo expression of functional α 2 -isoform of the catalytic subunit of rat Na + -K + -ATPase. (
  • ouabain and related cardiac glycosides are specific inhibitors of the Na + -K + -ATPase that catalyze the coupled active transport of Na + and K + across the plasma membrane of most higher eukaryotic cells ( 18 , 31 ). (
  • During simulated ischemia, cultured myocytes with enhanced expression of the human A3 receptor and showed significantly higher ATP content, fewer cells killed, and less creatine kinase released into the medium than either control or mock-transfected myocytes. (
  • Myocytes were then plated in 6-well dishes (1 × 10 6 cells/well) in a 5% CO 2 incubator and maintained in DMEM solution containing 20% fetal bovine serum/0.1 mM Brdu for an additional 72 h. (
  • The image analysis data is being used to investigate the effects that genetic modification have on how stem cells differentiate into cardiac myocytes and integrate into cardiac tissue. (
  • Antibodies against muscle-specific light meromyosin (anti-LMM) and desmin were used to distinguish cardiac myocytes from fibroblastic cells. (
  • These effects of HFCM are similar to the reported effects of hypoxia per se on these cell types, showing that hypoxic fibroblast-derived factors may amplify the distinct effects of hypoxia on cardiac cells. (
  • This variety of transcriptomic changes in infected mice raises the question of whether gene expression alterations in whole hearts are due to changes in infected cardiac myocytes or other cells or even to systemic effects of the infection on the heart. (
  • The cardiac action potential is a brief change in voltage (membrane potential) across the cell membrane of heart cells. (
  • The cardiac action potential differs from action potentials found in other types of electrically excitable cells, such as nerves. (
  • Unlike the action potential in skeletal muscle cells, the cardiac action potential is not initiated by nervous activity. (
  • All cardiac muscle cells are electrically linked to one another, by structures known as gap junctions (see below) which allow the action potential to pass from one cell to the next. (
  • Rate dependence of the action potential is a fundamental property of cardiac cells and alterations can lead to severe cardiac diseases including cardiac arrhythmia and sometimes sudden death. (
  • Following CRT we observed significant improvements in parameters of in vivo cardiac performance in HF dogs, including reduction in LV dimension and increased LV synchrony and fractional shortening. (
  • In addition, embryonic cardiac myocytes grown on the tubular substrate have an aligned phenotype that closely resembles in vivo neonatal ventricular myocytes. (
  • We propose that embryonic cardiac myocytes grown on the tube substrate develop into neonatal cardiac myocytes via normal in vivo mechanisms. (
  • Incubation of myocytes with exoenzyme C3 for 48 hours completely ADP-ribosylated Rho in vivo. (
  • We provide direct evidence for the first time of in vivo myocyte division in 6-wk-old chicken hearts. (
  • We used a microRNA antagomir and an AAV9 microRNA sponge delivery system to inhibit cardiac microRNA in vivo. (
  • Dexamethasone (Dex) pretreatment significantly increased cardiac contractile force ex vivo in Langendorff-perfused Sprague-Dawley rat hearts (2 mg/kg BW i.p. (
  • In accordance with our previous findings, HF myocytes exhibited characteristic reductions in the amplitude of the cytosolic Ca transients and sarcoplasmic reticulum (SR) Ca load and an increase in the frequency of spontaneous Ca sparks. (
  • Spontaneous calcium waves in cardiac myocytes are caused by diastolic sarcoplasmic reticulum release (SR Ca 2+ leak) through ryanodine receptors. (
  • Here, we show that in neonatal rat cardiac myocytes, beta-adrenergic stimulation generates multiple microdomains with increased concentration of cAMP in correspondence with the region of the transverse tubule/junctional sarcoplasmic reticulum membrane. (
  • The gene expression network of ion channels, SR and t-tubules genes was decoded using cutting edge genetic informatics on the ground experiment and found the appearance of many genes involved with calcium handling and myocyte maturation. (
  • Here, a novel maturation paradigm is created by culturing 3D cardiospheroids that enhances electrical maturation of the cardiac myocytes. (
  • These results suggest that chicken myocytes undergo hypertrophy and continue to proliferate during posthatching maturation, although it is currently believed that myocytes of all vertebrates withdraw from the cell cycle shortly after birth. (
  • Because cardiac myocytes possess a biosynthetic apparatus, including enzymes for elaborate propeptide processing, cardiac prohormone maturation has proven to be much more complex than initially assumed. (
  • Transfection of myocytes with JNK pathway interfering plasmid vectors or infection with adenoviral vectors support the hypothesis that JNK is protective. (
  • Astragaloside IV treatment could inhibit the PKCβ/Egr-1 pathway and protect against hypoxia/ reoxygenation-induced cardiac myocytes death, which contributes to improve our knowledge of mechanism in the cardioprotective function of Astragaloside IV. (
  • Conclusions- These data support the notion that sex-specific gene expression differences at baseline influence cardiac function, particularly through the protein kinase A pathway, and could potentially be responsible for differences in cardiovascular disease presentation and outcomes. (
  • High fructose causes cardiac hypertrophy via mitochondrial signaling pathway. (
  • A similar I was also observed in guinea pig cardiac myocytes. (
  • Block effects of IHC-72 on calcium current in single guinea pig cardiac myocytes. (
  • We are using integrative mathematical modelling to provide a framework within which to assess the quantitative contribution of different consequences of impaired metabolism to the overall deterioration of myocyte function during ischemia. (
  • We have applied this modelling framework to investigate the metabolic origins and functional consequences of several features of impaired myocyte physiology, including acidosis (Biophys J 90 3074 2006 ) and hyperkalemia (Am J Physiol 293 H3036 2007 ) arising over the first 15 minutes of zero flow ischemia, and subsequent calcium overload and calcium-dependent alternans (Terkildsen et al. (
  • Serious medical consequences of cocaine cardiotoxicity, including myocardial ischemia and infarction, ventricular fibrillation and sudden cardiac death, are serious health issues. (
  • Adenosine can achieve cardioprotection by mediating the effect of ischemic preconditioning and by protecting against myocyte injury when it is present during the infarct-producing ischemia. (
  • The objective of the present study was to investigate whether genetic manipulation of the cardiac myocyte, achieved by gene transfer and overexpression of the human A3 receptor cDNA, renders the myocytes resistant to the deleterious effect of ischemia. (
  • Prolonged hypoxia with glucose deprivation, causing myocyte injury and adenosine release, was used to simulate ischemia in cultured chick embryo ventricular myocytes. (
  • Overexpressing the adenosine A1 receptor also led to increased protection against ischemia-induced myocyte injury as well as an enhanced preconditioning effect. (
  • This is logical when one considers the nature of the acute coronarysyndrome, where in the vast majority of cases there is rupture of a plaque, leading to emboli causing cardiac myocyte ischemia and death. (
  • In many of these disorders, particularly those leading to chronic heart failure, myocyte cell death/loss is usually accompanied by an increase in fibrous tissue content (1). (
  • A novel method for simultaneously detecting multiple phospho-moieties of telethonin, based on Phos-tag phosphate affinity SDS-PAGE, was developed and used to reveal that endogenous telethonin exists predominantly in a dually-phosphorylated form in isolated adult rat ventricular myocytes (ARVM) and in ventricular tissue from rat and mouse hearts. (
  • In this study, we examined whether HK isoform differences could explain the markedly different metabolic profiles between normal adult and neonatal cardiac tissue. (
  • Recent electrophysiological, immunohistochemical, and dye-coupling data confirmed the presence of direct electrical coupling between the two cell types in normal cardiac tissue (sinoatrial node), and it has been suggested that similar interactions may occur in post-infarct scar tissue. (
  • Myocyte/fibroblast 2D structured cardiac tissue models. (
  • The goal of this study was to test the hypothesis that up-regulated expression of Spry1 in cardiac myocytes would be sufficient to inhibit ERK1/2 activation and tissue remodeling. (
  • In summary, targeted up-regulation of Spry1 in cardiac myocytes is not sufficient to alter cell or tissue remodeling consistent with the lack of an effect on ERK1/2 activity. (
  • Sedentary hypertensive rats had significant chamber dilatation and cardiac hypertrophy. (
  • Between the ages of 6 and 12 months in female spontaneously hypertensive heart failure (SHHF) rats, after a period of compensated hypertrophy, myocyte length begins to increase without further increase in CSA. (
  • The increased activity of pyruvate dehydrogenase (PDH) kinase induced in hearts of rats by starvation for 48 h was maintained following preparation of cardiac myocytes, and it was also maintained, though at a decreased level, after 25 h of culture in medium 199. (
  • The PDH kinase activity of myocytes from fed rats was increased to that of starved rats after 25 h of culture with n-octanoate, dibutyryl cyclic AMP or both agents together. (
  • Ventricular myocytes isolated from adult rats also responded specifically to PGF2 alpha with a morphological change similar to that observed with phenylephrine and by producing ANF . (
  • The transfusion of miR-208a-containing exosomes into normal rats resulted in worsened cardiac function. (
  • It may be anticipated that a rapid increase in our understanding of the pathophysiology of Ca2+ homeostasis in cardiac myocytes will be forthcoming as the powerful new tools of molecular and structural biology are used to investigate the regulation of Ca2+ transport systems. (
  • These results indicate that a novel I is present in mammalian heart and support a potentially important role of ClC-2 channels in the regulation of cardiac electrical activity and cell volume under physiological and pathological conditions. (
  • We investigated gene regulatory mechanisms involved in myocardial migration, and regulation of the timing of cardiac cone formation in zebrafish embryos. (
  • 1,25-Dihydroxyvitamin D3 regulation of cardiac myocyte proliferation and hypertrophy. (
  • L-type Ca2+ current in fish cardiac myocytes: effects of thermal acclimation and beta-adrenergic stimulation. (
  • Mechanisms of thin filament assembly in embryonic chick cardiac myocytes: tropomodulin requires tropomyosin for assembly. (
  • The topographical relationship between stress fiber-like structures (SFLS) and nascent myofibrils was examined in cultured chick cardiac myocytes by immunofluorescence microscopy. (
  • Primary Human Cardiac Myocytes isolated from the ventricles of the adult heart. (
  • Collectively, these results suggest that carnosine protects cardiac myocytes against HNE and acrolein toxicity by directly reacting with these aldehydes. (
  • Cellular cardiac electrophysiology modeling with Chaste and CellML. (
  • This review illustrates that it would be wrong to adhere to a scenario of functional integration of the heart that does not allow for a potential active contribution of non-myocytes to cardiac electrophysiology, and proposes to focus further research on the relevance of non-myocytes for cardiac structure and function. (
  • Under conditions in which cationic inward rectifier channels were blocked, membrane hyperpolarization (−40 to −140 mV) activated an inwardly rectifying whole-cell current in mouse atrial and ventricular myocytes. (
  • They also found that I K(ACh) is present in both atrial and ventricular myocytes. (
  • Herein, I show that cocaine, in pharmacological doses, selectively and potently enhances L-type calcium channel currents in isolated rat ventricular myocytes. (
  • Moreover, Ca transient amplitude as well as fractional shortening were significantly enhanced in Fura-2-loaded isolated rat ventricular myocytes exposed to Dex (1 mg/mL Dex, 24 h). (
  • Brunton LL, Hayes JS, Mayer SE (1979) Hormonally specific phosphorylation of cardiac troponin I and activation of glycogen phosphorylase. (
  • CKD patients with advanced disease have misfortune of having both a dramatically high rate of cardiac mortality paired with decreased ability to detect, it due to elevated Cardiac Troponin levels. (
  • Treatment of myocytes with Ang II caused a rapid formation of both striated (mature myofibrils) and nonstriated (premyofibrils) actin fibers within 30 minutes, as determined by phalloidin stainings of the polymerized actin and troponin T stainings. (
  • We developed CRISPR/Cas9/AAV9-based somatic mutagenesis, a platform in which AAV9 delivers tandem guide RNAs targeting a gene of interest and cardiac troponin-T promoter-driven Cre to RosaCas9GFP/Cas9GFP neonatal mice. (
  • Is it time to do away with the 99th percentile for cardiac troponin in the diagnosis of acute coronary syndrome and the assessment of cardiac risk? (
  • To evaluate the role of inducible nitric oxide synthase (iNOS) on cardiac myocyte cytotoxicity, we exposed adult rat cardiac myocytes to either cytokines alone or to activated J774 macrophages in coculture. (
  • We examined the activation of mitogen- and stress-activated protein kinase-1 (MSK1), a downstream target of MAPKs, in adult rat cardiac myocytes by phenylephrine and endothelin-1. (
  • According to one study just 21% of 48 athletes who died of hypertrophic cardiomyopathy related sudden death had previous signs or symptoms of cardiac disease (chest pain, exertional dyspnea, syncope, dizziness) before death (Koester, 2001). (
  • Although Rho-family small G proteins have been implicated in actin organization in many cell types, it is not fully elucidated whether Rho mediates the organization of actin fibers by hypertrophic stimuli in cardiac myocytes. (
  • Therefore, we examined (1) whether Rho is activated by the hypertrophic stimulus, angiotensin II (Ang II), and (2) whether Rho mediates the Ang II-induced organization of actin fibers in cultured neonatal rat cardiac myocytes. (
  • Ang II activates multiple second-messenger systems in cardiac myocytes, 16 and each signaling molecule seems to mediate distinct hypertrophic responses. (
  • An encouraging recent study by Konhilas et al 9 found that voluntary wheel running (VWR) resulted in reduced myocyte disruption, beneficial changes in apoptotic markers, and reversal of fetal genes in hypertrophic cardiomyopathic mice. (
  • Molecular mechanisms of angiotensin II in modulating cardiac function: intracardiac effects and sign. (
  • We have previously shown that epidermal growth factor (EGF) augments cAMP accumulation in the heart and stimulates cardiac adenylyl cyclase via a G protein mediated mechanism (Nair et al. (
  • 7 Cardiac hypertrophy is also characterized by the induction of immediate-early genes (eg, c- fos and c- jun ), activation of the fetal gene program (eg, ANF and skeletal α-actin), and increases in protein synthesis and cell size (reviewed in References 7 7 to 11). (
  • Increased expression of both iNOS message and protein was seen in J774 macrophages treated with IFN gamma and LPS and cardiac myocytes treated with TNF-alpha, IL-1 beta, and IFN gamma. (
  • TGF-beta reduced expression of cardiac myocyte iNOS message and protein, reduced nitrite production, and reduced NO-mediated cytotoxicity in parallel. (
  • The titin-cap protein telethonin was previously identified by our group as an interaction partner for the protein kinase D (PKD) catalytic domain, through a yeast two-hybrid screen of a human cardiac cDNA library. (
  • Expression of Foxp1 protein during cardiac development. (
  • G-protein-coupled receptor agonists are powerful stimulators of mitogen-activated protein kinase (MAPK) cascades in cardiac myocytes. (
  • Myocytes exposed to this prostanoid in culture increased in size and protein content. (
  • His blood test results reveal (cardiac markers): elevated troponins and creatine kinase (CK) and lipid panel: high cholesterol, high low-density lipoprotein (LDL), low high-density lipoprotein (HDL). (
  • Focal adhesion kinase (FAK) has been shown to be activated in cardiac myocytes exposed to mechanical stress. (
  • We recently showed ( 12 , 39 ) that FAK activation by mechanical stress is accompanied by its aggregation at myofilaments, Z disks, and costameres, implying that this kinase might be directly activated by mechanical stress in cardiac myocytes. (
  • In this study, we used a neonatal rat ventricular myocyte (NRVM) model to determine the role of focal-adhesion kinase (FAK) in β 1 integrin mediated MAP kinase activation in response to mechanical stretch in presence and absence of Ang II receptor blockade (ATB). (
  • Cardiac-specific myosin light chain kinase (cMLCK) is the kinase predominantly responsible for the maintenance of the basal level of phosphorylation of cardiac myosin light chain 2 (MLC2), which it phosphorylates at Ser-15. (
  • The lethal effects of cytokine-induced nitric oxide on cardiac myocytes are blocked by nitric oxide synthase antagonism or transforming growth factor beta. (
  • Cripto also affects the formation of nitric oxide, a small signaling molecule that has been reported to be important for growth and development of cardiac and smooth muscle. (
  • The present study examined whether nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) can directly inhibit aerobic energy metabolism and impair cell function in interleukin (IL)-1β-stimulated cardiac myocytes. (
  • Critically, in myocytes isolated from nitric oxide synthase 1 knock-out mice this effect is ablated. (
  • Gene expression profiling of the aging mouse cardiac myocytes. (
  • Extracellular ATP induces immediate early gene expression but not cellular hypertrophy in neonatal cardiac myocytes. (
  • Hypoxia-induced expression of heme-oxygenase gene expression in cultured neonatal rat cardiac myocytes. (
  • Statistical comparison of gene expression levels of 7624 well annotated unigenes in four independent cultures of infected and uninfected myocytes detected substantial (≥1.5 absolute fold changes) in 420 (5.5%) of the sampled genes. (
  • The thromboxane A2 mimic U46619 increases calcium transients in rat cardiac myocytes. (
  • Block of the calcium current by IHC-72 in single ventricular myocytes isolated from guinea pig was studied by using the whole-cell patch clamp technique. (
  • In ventricular myocytes isolated from wild-type mice, isoproterenol stimulation also increased the CaMKII-dependent leak. (
  • The authors of this week's paper used single molecule localization super resolution microscopy to study the effect of cardiac failure on the sarcomeric cytoskeleton after cardiac failure. (
  • 1. Fluo-3 fluorescence measurements were made in isolated beta -escin permeablised rat cardiac myocytes using confocal microscopy. (
  • Organization of actin fibers into myofibrils is one of the major characteristics of cardiac hypertrophy, a growth response observed in terminally differentiated cardiac myocytes. (
  • The relationship between stress fiber-like structures and nascent myofibrils in cultured cardiac myocytes. (
  • and (d) in regions of a myocyte with numerous mature myofibrils, SFLS had totally disappeared. (
  • Lastly, it is of considerable theoretical interest to note that mature cardiac myocytes, like mature skeletal myotubes, lack readily detectable stress fibers. (
  • No significant cytotoxic or apoptotic effects were observed on cardiac myocytes after 24 and 48 h of exposure with concentrations up to 200 μg/mL. (
  • The underlying mechanisms contributing to improved cardiac function remain poorly understood. (
  • To evaluate mechanisms of β-blocker efficacy, we extended our cardiac myocyte β1-adrenergic signaling model using an extended ternary complex receptor model. (
  • Elucidating the molecular mechanisms of action of cocaine, therefore, remains a critical step in developing treatment for cocaine addiction and preventing cardiac complications. (
  • We measured cardiac-specific microRNA levels in two rat models of cardiac fibrosis to find out which microRNA was involved in the common mechanisms of cardiac fibrosis. (
  • Syngene has announced that the G:BOX Chemi XRQ high resolution, multi-application image analysis system is being successfully used at the Lithuanian University of Health Sciences Academy of Medicine to study molecular mechanisms of cardiac stem cell function which could help in developing stem cell therapies for heart repair. (
  • Key genes in heart development are homologous between insects and mammals (e.g. tinman), as are key components of cardiac myocyte physiology, including ion channels, pumps and exchangers. (
  • Brittsan AG, Kranias EG (2000) Phospholamban and cardiac contractile function. (
  • We describe a computational framework for the comprehensive assessment of contractile responses of enzymatically dissociated adult cardiac myocytes. (
  • In contractile myocytes, photorelease of NAADP caused significant increase in calcium transient amplitude and velocity of transient upstroke and decay. (
  • Conversely, inhibition of cardiac myocyte death in this murine model largely prevents the development of cardiac dilation and contractile dysfunction, the hallmarks of heart failure. (
  • Therefore, tertiapin potently and selectively blocks the K ACh channel in cardiac myocytes in a receptor- and voltage-independent manner. (
  • Thus, increasing the receptor level improves the myocyte sensitivity to the endogenous adenosine, which in turn causes all of the cardioprotective effects found for exogenously administered adenosine agonists. (
  • The study provides the first proof for the new concept that an increased expression of the human A3 receptor in the cardiac myocyte can be an important cardioprotective therapeutic approach. (
  • Transcripts for HGF ligand and receptor are first detected before cardiac function and looping and persist through the first looping stage, when heart morphology begins to elaborate. (
  • HGF ligand and receptor mRNA are detectable after the putative heart transcription factor, Csx/Nkx2-5, and concomitantly with the heart structural gene, cardiac actin. (
  • In addition to evoking spontaneous Ca2+ transients, stimulation of ventricular myocytes with the Ins(1,4,5)P-3 ester caused a positive inotropic effect. (
  • In cardiac myocytes and many other cell types, however, cAMP transduces the signal generated upon stimulation of various receptors and activates different cellular functions, raising the issue of how specificity can be achieved. (
  • Reverse transcription polymerase chain reaction and Northern blot analysis confirmed transcriptional expression of ClC-2 in both atrial and ventricular tissues and isolated myocytes of mouse and guinea pig hearts. (
  • This is primarily for detection of risk of Torsade-de-Pointes (TdP) cardiac arrhythmia. (
  • The metabolics and calcium handling properties of the reprogramed myocyte flown in space are then tested for their improved potential for repairing a damaged mouse heart model on earth. (
  • Cardiac resynchronization therapy (CRT) represents a promising treatment modality to alleviate LV dysfunction in humans with heart failure (HF). (
  • 1990). Since the heart comprises of a variety of cell types, the purpose of the studies presented here was to determine whether or not the effects of EGF on adenylyl cyclase were mediated in cardiac myocytes or noncardiomyocytes. (
  • Intriguingly, expression of both IP 3 Rs and membrane receptors that couple to PLC/IP 3 signaling is altered in cardiac disease such as atrial fibrillation or heart failure, suggesting the involvement of IP 3 signaling in the pathology of these diseases. (
  • The long-term effects of exercise on cardiac function and myocyte remodeling in hypertension/progression of heart failure are poorly understood. (
  • We conclude that excessive exercise, in the untreated hypertensive state can have deleterious effects on cardiac remodeling and may actually accelerate the progression to heart failure. (
  • Research has shown a predictable remodeling of cardiac myocyte shape underlying progression to heart failure (HF). (
  • Because muscarinic receptors play a crucial role in modulation of heart rate and stabilization of membrane electrical excitability ( Billman and Hoskins, 1989 ), it is important to evaluate the effects of cocaine on cardiac I K(ACh) . (
  • It has also been pointed out ( 28 , 29 ) that the reduced Na + -K + -ATPase of the failing heart may exacerbate toxicity of cardiac glycosides in the diseased heart, because the toxic effects of these drugs are known to be the extension of their therapeutic effects. (
  • Preconditioning and Postconditioning by Cardiac Glycosides in the Mouse Heart. (
  • Heart weight and cardiac myocyte morphology were unchanged in adult male α-MHC-Spry1 mice compared to control mice. (
  • In the heart, the second messengers cAMP and cGMP mediate the effects of several hormones and neurotransmitters, regulating cardiac function and are the target of key drugs used to treat heart conditions. (
  • Cardiac Cell Therapy Rejuvenates the Infarcted Rodent Heart via Direct Injection but Not by Vascular Infusion. (
  • Increased NO synthesis was associated with a parallel increase in myocyte death as measured by CPK release into the culture medium as well as by loss of membrane integrity, visualized by trypan blue staining. (
  • 1 Initially, under hypertensive conditions, there is a marked increase in myocyte cross-sectional area (CSA) whereas cell length remains normal. (
  • We used a set of novel genetically encoded optical imaging tools to track, in real-time in isolated adult (ARVM) and neonatal (NRVM) rat ventricular myocytes, the subcellular distributions of HKI and HKII, and the functional consequences on glucose utilization. (
  • Shortly after birth, cardiac myocytes switch from predominant expression of HKI and the glucose transporter GLUT1 to the insulin-sensitive isoforms HKII and GLUT4. (
  • The myocytes showed a concomitant significant increase in glucose consumption, a marked increase in lactate production, and a significant decrease in cellular ATP (adenosine 5′-triphosphate). (
  • Of the 11 families of phosphodiesterases found in the human genome, three decades of pharmacological data have clearly implicated PDE3 in cardiac function. (
  • In this chapter, the molecular properties and function of PDE4s in the different compartments of the cardiac myocytes will be reviewed. (
  • Therefore, long-term preservation or enhancement of cardiac function depends on structural adaptation. (
  • It is important for future studies to elucidate how cross talk between these mechanical signals is coordinated to control myocyte structure and function. (
  • Using the same HF model, we now show that CRT resynchronization therapy reverses this defective RyR function and normalizes Ca handling in myocytes from failing hearts. (
  • Excessive fibrosis in the presence of myocyte loss has been advocated as a basis for impaired myocardial function in these disease states. (
  • Exercise did not significantly impact myocyte remodeling or ventricular function in control animals. (
  • These data indicate that I K(ACh) is present in ventricular myocytes and may play important roles in cardiac function. (
  • Loss-of-function studies in cardiac myocytes (CMs) are currently limited by the need for appropriate conditional knockout alleles. (
  • Multiple cAMP phosphodiesterase (PDE) isoforms play divergent roles in cardiac homeostasis but the molecular basis for their non-redundant function remains poorly understood. (
  • Together, these findings indicate that plasma miR-208 is a cardiac-specific biomarker that reflects the extent of cardiac myocyte injury but isnotsubstantially influenced by antecedent cardiac hypertrophy, renal function, or cellular injury involving other organs. (
  • At least six distinct types of sarcolemmal Cl − currents have been functionally identified in cardiac myocytes. (
  • We examined the effect of tertiapin on ion channel currents in rabbit cardiac myocytes using the patch-clamp technique. (
  • In the whole-cell configuration, tertiapin fully inhibited acetylcholine (1 μM)-induced muscarinic K + (K ACh ) channel currents in atrial myocytes with the half-maximum inhibitory concentration of ∼8 nM through ∼1:1 stoichiometry. (
  • Accumulating evidence suggests that steady-state K + currents modulate excitability and action potential duration, particularly in cardiac cell types with relatively abbreviated action potential plateau phases. (
  • We established a murine model with up-regulated Spry1 expression in cardiac myocytes using the alpha-myosin heavy chain promoter (α-MHC). (