Search results for "Cardiomyocyte"

showing 10 items of 20 documents

Impaired Binding to Junctophilin-2 and Nanostructural Alteration in CPVT Mutation

2021

Rationale: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare disease, manifested by syncope or sudden death in children or young adults under stress conditions. Mutations in the Ca 2+ release channel/RyR2 (type 2 ryanodine receptor) gene account for about 60% of the identified mutations. Recently, we found and described a mutation in RyR2 N-terminal domain, RyR2 R420Q . Objective: To determine the arrhythmogenic mechanisms of this mutation. Methods and Results: Ventricular tachycardias under stress conditions were observed in both patients with catecholaminergic polymorphic ventricular tachycardia and knock-in mice. During action potential recording (by patch-clamp in …

Ile de francePhysiologyCPVT030204 cardiovascular system & hematologyArticle03 medical and health sciences0302 clinical medicineaction potential[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemPolitical sciencejunctophilinryanodine receptormedia_common.cataloged_instanceHumansEuropean union610 Medicine & health030304 developmental biologymedia_common0303 health sciencescalciumRyanodine Receptor Calcium Release ChannelRyR2musculoskeletal systemSarcoplasmic ReticulumDeath Sudden Cardiaccalcium induced calcium releaseGain of Function Mutationcardiomyocyte calcium handlingcardiovascular systemventricular tachycardiamutationCardiology and Cardiovascular MedicineHumanities
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MiR-133 Modulates the β1Adrenergic Receptor Transduction Cascade.

2014

Rationale : The sympathetic nervous system plays a fundamental role in the regulation of myocardial function. During chronic pressure overload, overactivation of the sympathetic nervous system induces the release of catecholamines, which activate β-adrenergic receptors in cardiomyocytes and lead to increased heart rate and cardiac contractility. However, chronic stimulation of β-adrenergic receptors leads to impaired cardiac function, and β-blockers are widely used as therapeutic agents for the treatment of cardiac disease. MicroRNA-133 (miR-133) is highly expressed in the myocardium and is involved in controlling cardiac function through regulation of messenger RNA translation/stability. …

MalePhysiologyMessengerheart failureApoptosiscardiomyocytesInbred C57BLSecond Messenger SystemsTransgenicRats Sprague-DawleyBeta-1 adrenergic receptorMiceGenes ReporterReceptorsCyclic AMPGuanine Nucleotide Exchange FactorsMyocytes CardiacAlpha-1D adrenergic receptor3' Untranslated RegionsCells CulturedCulturedbiologyChemistryadrenergic beta-1 receptor antagonists; cardiac; cyclic AMP; heart failure; microRNAs; myocytes; 3' Untranslated Regions; Adenylyl Cyclases; Animals; Apoptosis; Cells Cultured; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Disease Progression; Gene Expression Regulation; Genes Reporter; Guanine Nucleotide Exchange Factors; Male; Metoprolol; Mice; Mice Inbred C57BL; Mice Transgenic; MicroRNAs; Myocardium; Myocytes Cardiac; RNA Messenger; Rats; Rats Sprague-Dawley; Receptors Adrenergic beta-1; Recombinant Fusion Proteins; Second Messenger Systems; Physiology; Cardiology and Cardiovascular Medicine; Medicine (all)Medicine (all)Cell biologyAdrenergicadrenergic beta-1 receptor antagonistsDisease ProgressionCARDIAC HYPERTROPHYSignal transductionCardiology and Cardiovascular MedicineAdenylyl CyclasesMetoprololmedicine.medical_specialtyAdrenergic receptorcardiacCellsRecombinant Fusion ProteinsMice Transgenicbeta-1Alpha-1B adrenergic receptorInternal medicinecAMPmedicineAnimalsRNA MessengerReporterPressure overloadalpha and beta adrenoceptorsMyocytesMyocardiumBeta adrenergic receptor kinaseCyclic AMP-Dependent Protein KinasesAlpha-1A adrenergic receptorRatsMice Inbred C57BLMicroRNAsEndocrinologyGenesGene Expression Regulationbiology.proteinRNASprague-DawleyReceptors Adrenergic beta-1MicroRNAs; alpha and beta adrenoceptors; cardiomyocytes; CARDIAC HYPERTROPHY; cAMP
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Isolation and Characterization of CD276+/HLA-E+ Human Subendocardial Mesenchymal Stem Cells from Chronic Heart Failure Patients: Analysis of Differen…

2012

Mesenchymal stem cells (MSCs) are virtually present in all postnatal organs as well as in perinatal tissues. MSCs can be differentiated toward several mature cytotypes and interestingly hold potentially relevant immunomodulatory features. Myocardial infarction results in severe tissue damage, cardiomyocyte loss, and eventually heart failure. Cellular cardiomyoplasty represents a promising approach for myocardial repair. Clinical trials using MSCs are underway for a number of heart diseases, even if their outcomes are hampered by low long-term improvements and the possible presence of complications related to cellular therapy administration. Therefore, elucidating the presence and role of MS…

Pathologymedicine.medical_specialtyB7 AntigensHeart VentriclesGene ExpressionCell SeparationBiologyCell therapyHLA-EAntigens CDOsteogenesisCellular cardiomyoplastymedicineHumansImmunologic FactorsMyocardial infarctionCells CulturedHeart FailureAdipogenesisMesenchymal stem cells human heart stromal progenitors post-infarct chronic heart failure cardiomyocyte markers immune modulation inflammation cardiac remodelling regenerative medicineSettore BIO/16 - Anatomia UmanaHistocompatibility Antigens Class IMesenchymal stem cellMesenchymal Stem CellsCell BiologyHematologyAnatomymedicine.diseaseClinical trialmedicine.anatomical_structureVentricleHeart failureChondrogenesisBiomarkersDevelopmental BiologyStem Cells and Development
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Heat Shock Protein-60 and Risk for Cardiovascular Disease

2011

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. There is growing evidence that molecularchaperones, many of which are heat shock proteins HSPs, are involved in CVD pathogenesis. In this review we focus on HSP60,the human mitochondrial chaperone that also displays extramitochondrial and extracellular functions. HSP60 is typically cytoprotectivebut a number of stress conditions determine its conversion to a potentially toxic molecule for cells and tissues. We present illustrative examplesof specific subtypes of CVD where HSP60 is implicated in the initiation and/or progression of disease. The data not only indicatea pathogenic role for HSP60 but also its …

Riskanimal structuresChaperonin Heat shock protein-60 cardiomyocytes heart failure cardiovascular diseases atherosclerosisChaperonin heat shock protein 60 cardiomyocytes heart failure cardiovascular disease atherosclerosis apoptosis microRNAs (miRs) diabetes Atrial fibrillationApoptosischemical and pharmacologic phenomenaDiseaseBioinformaticsAutoimmune DiseasesPathogenesisHeat shock proteinAtrial FibrillationDrug DiscoveryExtracellularAnimalsHumansMyocytes CardiacHeart FailurePharmacologybiologyfungiChaperonin 60AtherosclerosisResponse to treatmentCardiovascular DiseasesReperfusion InjuryChaperone (protein)HypertensionImmunologybiology.proteinHSP60Stress conditionsBiomarkersCurrent Pharmaceutical Design
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In vitro simulation of spiral waves in cardiomyocyte networks using multi-electrode array technology

2009

International audience; We aimed thus to provide new insights into the cellular origin of the fibrillation phenomenon by exploring the impulse propagation between cardiac myocytes in confluent monolayers of cultured cardiomyocytes (CM),

[SDV.MHEP] Life Sciences [q-bio]/Human health and pathology[ INFO.INFO-TS ] Computer Science [cs]/Signal and Image Processing[INFO.INFO-TS] Computer Science [cs]/Signal and Image Processing[ NLIN.NLIN-CD ] Nonlinear Sciences [physics]/Chaotic Dynamics [nlin.CD][ SPI.SIGNAL ] Engineering Sciences [physics]/Signal and Image processingmulti electrode arraycardiomyocytes network[NLIN.NLIN-CD] Nonlinear Sciences [physics]/Chaotic Dynamics [nlin.CD][INFO.INFO-TS]Computer Science [cs]/Signal and Image Processing[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathology[NLIN.NLIN-CD]Nonlinear Sciences [physics]/Chaotic Dynamics [nlin.CD]spiral waves[SPI.SIGNAL]Engineering Sciences [physics]/Signal and Image processing[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology[SPI.SIGNAL] Engineering Sciences [physics]/Signal and Image processing
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Synthetic/ECM-inspired hybrid platform for hollow microcarriers with ROS-triggered nanoporation hallmarks

2017

Reactive oxygen species (ROS) are key pathological signals expressed in inflammatory diseases such as cancer, ischemic conditions and atherosclerosis. An ideal drug delivery system should not only be responsive to these signals but also should not elicit an unfavourable host response. This study presents an innovative platform for drug delivery where a natural/synthetic composite system composed of collagen type I and a synthesized polythioether, ensures a dual stimuli-responsive behaviour. Collagen type I is an extracellular matrix constituent protein, responsive to matrix metalloproteinases (MMP) cleavage per se. Polythioethers are stable synthetic polymers characterized by the presence o…

biomedical applicationsPathologyresponsivenessPolymersNanoparticlecardiomyocytes02 engineering and technologyMatrix metalloproteinaseMicroscopy Atomic Force01 natural sciencesreleaseHollow spheresExtracellular matrixDrug Delivery Systemsreactive oxygenCytotoxicitynanomaterialsdegradationchemistry.chemical_classificationDrug CarriersMicroscopyMultidisciplinaryIschemic conditionsQRAtomic ForcePolymerStimuli-responsive021001 nanoscience & nanotechnologyMicrospheresDrug deliveryMedicineROS (Reactive Oxygen Species) inflamed tissue stimuli-responsive biomaterials ischemic conditions hollow spheres polysulfides collagenCollagenhypoxia-reoxygenationdelivery0210 nano-technologyAnimals; Cell Line; Drug Carriers; Drug Delivery Systems; Matrix Metalloproteinases; Microscopy Atomic Force; Microspheres; Polymers; Rats; Reactive Oxygen Speciesmedicine.medical_specialtyROS (Reactive Oxygen Species)ScienceInflamed tissue010402 general chemistryArticleCell LineBiomaterialsPolysulfidesmedicineAnimalsReactive oxygen speciesMicrocarrierMatrix Metalloproteinases0104 chemical sciencesRatschemistrySettore CHIM/09 - Farmaceutico Tecnologico ApplicativoBiophysicsnanoparticlesReactive Oxygen Species
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STAT5b is a key effector of NRG-1/ERBB4-mediated myocardial growth

2023

The growth factor Neuregulin-1 (NRG-1) regulates myocardial growth and is currently under clinical investigation as a treatment for heart failure. Here, we demonstrate in several in vitro and in vivo models that STAT5b mediates NRG-1/EBBB4-stimulated cardiomyocyte growth. Genetic and chemical disruption of the NRG-1/ERBB4 pathway reduces STAT5b activation and transcription of STAT5b target genes Igf1, Myc, and Cdkn1a in murine cardiomyocytes. Loss of Stat5b also ablates NRG-1-induced cardiomyocyte hypertrophy. Dynamin-2 is shown to control the cell surface localization of ERBB4 and chemical inhibition of Dynamin-2 downregulates STAT5b activation and cardiomyocyte hypertrophy. In zebrafish e…

cardiomyocyte hypertrophyNRG-1–ErbB pathwaygeenitsydäncardiomyocyte hyperplasiadynaminkasvutekijätsydänlihassairaudetsydänlihassoluthypertrofinen kardiomyopatiasignal transduceractivator of transcriptionsolufysiologia
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Isolation of Adult Rat Cardiomyocytes Using Recombinant Collagenases

2018

Direct isolation of primary cells from tissues and organs allows for the maintenance of important cell characteristics and properties for in vitro studies and a plethora of biomedical applications. Dissociation of cells from the organ of interest is possible due to the enzymatic activity of collagenases. The choice and the dose of these enzymes is the critical step to obtain the maximum number of cells with intact structure and function. In this contest, Abiel collagenases class I (Col G) and class II (Col H) were synthesised using recombinant DNA technologies and their ability to degrade collagen in cell isolation from different tissues was tested. Examples of cells isolated with these enz…

cell isolationlcsh:Computer engineering. Computer hardwarecollagenaseslcsh:TP155-156cardiomyocytelcsh:TK7885-7895lcsh:Chemical engineeringChemical Engineering Transactions
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Cytoskeleton mediates negative inotropism and lusitropism of chromogranin A-derived peptides (human vasostatin1-78 and rat CgA(1-64)) in the rat heart

2010

Cytoskeleton scaffold in cardiac myocytes provides structural support and compartmentalization of intracellular components. It is implicated in cardiac pathologies including hypertrophy and failure, playing a key role in the determinism of contractile and diastolic dysfunctions. Chromogranin A (CgA) and its derived peptides have revealed themselves as novel cardiovascular modulators. In humans, normal CgA levels considerably increase in several pathologies, including heart failure. Recent data have shown on the unstimulated rat heart that human recombinant Vasostatin-1 (hrVS-1) and rat chromogranin A 1-64 (rCgA(1-64)) induce negative inotropic and lusitropic effects counteracting the beta-a…

medicine.medical_specialtyMESH: RatsPhysiologyPhalloidin[SDV]Life Sciences [q-bio]Clinical BiochemistryMESH: Myocytes Cardiacmacromolecular substancesBiologyBiochemistryWortmanninCellular and Molecular Neurosciencechemistry.chemical_compoundEndocrinologyInternal medicineMyosinmedicineMESH: CytoskeletonMyocyteMESH: AnimalsCytoskeletonActinMESH: In Vitro TechniquesMESH: HumansSettore BIO/16 - Anatomia UmanaChromogranin AMESH: Rats WistarMESH: MaleCell biologyMESH: Cell LineMESH: Heart[SDV] Life Sciences [q-bio]EndocrinologychemistryInotropismVasostatin Rat CgA1-64 Rat Langendorff heart Inotropy Lusitropy Cardiomyocytes Cytoskeletonbiology.proteinMESH: Chromogranin A
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Endothelial Bmx tyrosine kinase activity is essential for myocardial hypertrophy and remodeling

2015

Cardiac hypertrophy accompanies many forms of heart disease, including ischemic disease, hypertension, heart failure, and valvular disease, and it is a strong predictor of increased cardiovascular morbidity and mortality. Deletion of bone marrow kinase in chromosome X (Bmx), an arterial nonreceptor tyrosine kinase, has been shown to inhibit cardiac hypertrophy in mice. This finding raised the possibility of therapeutic use of Bmx tyrosine kinase inhibitors, which we have addressed here by analyzing cardiac hypertrophy in gene-targeted mice deficient in Bmx tyrosine kinase activity. We found that angiotensin II (Ang II)-induced cardiac hypertrophy is significantly reduced in mice deficient i…

medicine.medical_specialtyendotheliumEndotheliumAngiogenesiscardiomyocyteCardiomegalyheartmTORC1030204 cardiovascular system & hematologyMitochondria Heart03 medical and health sciencesMice0302 clinical medicineInternal medicinemedicineAnimalsMyocytes Cardiac030304 developmental biologyMice Knockout0303 health sciencesMultidisciplinaryKinasebusiness.industryta1184Angiotensin IIBiological SciencesProtein-Tyrosine KinasesAngiotensin IImedicine.anatomical_structureEndocrinologyEtkcardiovascular systemCancer researchPhosphorylationCytokinesEndothelium VascularSignal transductionInflammation MediatorssignalingbusinessTyrosine kinaseSignal Transduction
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