Search results for "Myocytes"

showing 10 items of 117 documents

Arsenic trioxide alters the differentiation of mouse embryonic stem cell into cardiomyocytes

2015

AbstractChronic arsenic exposure is associated with increased morbidity and mortality for cardiovascular diseases. Arsenic increases myocardial infarction mortality in young adulthood, suggesting that exposure during foetal life correlates with cardiac alterations emerging later. Here, we investigated the mechanisms of arsenic trioxide (ATO) cardiomyocytes disruption during their differentiation from mouse embryonic stem cells. Throughout 15 days of differentiation in the presence of ATO (0.1, 0.5, 1.0 μM) we analysed: the expression of i) marker genes of mesoderm (day 4), myofibrillogenic commitment (day 7) and post-natal-like cardiomyocytes (day 15); ii) sarcomeric proteins and their orga…

Fetal ProteinsSarcomeresMesodermTime FactorsCellular differentiationBlotting WesternConnexinFluorescent Antibody TechniqueGene ExpressionAntineoplastic AgentsActininBiologyArticleArsenicalsCell Linechemistry.chemical_compoundMiceArsenic TrioxideTroponin TSpheroids CellularGene expressionmedicineAnimalsActininMyocytes CardiacArsenic trioxideHomeodomain ProteinsSyncytiumMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionCell DifferentiationMouse Embryonic Stem CellsOxidesEmbryonic stem cellCell biologyBiomechanical PhenomenaGATA4 Transcription Factormedicine.anatomical_structurechemistryConnexin 43ImmunologyHomeobox Protein Nkx-2.5T-Box Domain ProteinsTroponin CTranscription FactorsScientific Reports
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Telmisartan cardioprotects from the ischaemic/hypoxic damage through a miR‐1‐dependent pathway

2019

The aim of this study was to investigate whether telmisartan protects the heart from the ischaemia/reperfusion damage through a local microRNA-1 modulation. Studies on the myocardial ischaemia/reperfusion injury in vivo and on the cardiomyocyte hypoxia/reoxygenation damage in vitro were done. In vivo, male Sprague-Dawley rats administered for 3 weeks with telmisartan 12 mg/kg/d by gastric gavage underwent ischaemia/reperfusion of the left descending coronary artery. In these rats, infarct size measurement, ELISA, immunohistochemistry (IHC) and reverse transcriptase real-time polymerase chain reaction showed that expressions of connexin 43, potassium voltage-gated channel subfamily Q member …

Male0301 basic medicineCell SurvivalMyocardial InfarctionIschemiaConnexinMyocardial Reperfusion InjuryPharmacologymiR‐1telmisartanCell Lineconnexin 43Rats Sprague-Dawleyhypoxic H9c2 cells03 medical and health sciences0302 clinical medicineIn vivomedicineAnimalsBcl-2Myocytes CardiacKCNQ1ChemistryBcl‐2Original ArticlesCell BiologyTransfectionHypoxia (medical)medicine.diseasemiR-1Cell HypoxiaIn vitroRatsMicroRNAsmyocardial ischaemia/reperfusion030104 developmental biologyProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisKCNQ1 Potassium ChannelMolecular Medicinehypoxic H9c2 cellOriginal Articlemedicine.symptomTelmisartanReperfusion injurymedicine.drugJournal of Cellular and Molecular Medicine
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Investigating and re-evaluating the role of glycogen synthase kinase 3 beta kinase as a molecular target for cardioprotection by using novel pharmaco…

2019

Aims Glycogen synthase kinase 3 beta (GSK3β) link with the mitochondrial Permeability Transition Pore (mPTP) in cardioprotection is debated. We investigated the role of GSK3β in ischaemia (I)/reperfusion (R) injury using pharmacological tools. Methods and results Infarct size using the GSK3β inhibitor BIO (6-bromoindirubin-3'-oxime) and several novel analogues (MLS2776-MLS2779) was determined in anaesthetized rabbits and mice. In myocardial tissue GSK3β inhibition and the specificity of the compounds was tested. The mechanism of protection focused on autophagy-related proteins. GSK3β localization was determined in subsarcolemmal (SSM) and interfibrillar mitochondria (IFM) isolated from Lang…

Male0301 basic medicinePhysiologyMyocardial InfarctionAutophagy-Related ProteinsMyocardial Reperfusion Injury030204 cardiovascular system & hematologyMitochondrionPharmacologyMitochondrial Membrane Transport ProteinsMitochondria HeartStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineReperfusion therapyPhysiology (medical)AnimalsMyocytes CardiacProtein Kinase InhibitorsGSK3BMice Knockoutchemistry.chemical_classificationCardioprotectionReactive oxygen speciesGlycogen Synthase Kinase 3 betaMolecular StructureMitochondrial Permeability Transition PoreChemistryKinaseMPTPIsolated Heart PreparationMice Inbred C57BLDisease Models Animal030104 developmental biologyMitochondrial permeability transition poreFemaleRabbitsCardiology and Cardiovascular MedicineCyclophilin DSignal TransductionCardiovascular Research
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Stable Oxidative Cytosine Modifications Accumulate in Cardiac Mesenchymal Cells From Type2 Diabetes Patients

2018

Rationale: Human cardiac mesenchymal cells (CMSCs) are a therapeutically relevant primary cell population. Diabetes mellitus compromises CMSC function as consequence of metabolic alterations and incorporation of stable epigenetic changes. Objective: To investigate the role of α-ketoglutarate (αKG) in the epimetabolic control of DNA demethylation in CMSCs. Methods and Results: Quantitative global analysis, methylated and hydroxymethylated DNA sequencing, and gene-specific GC methylation detection revealed an accumulation of 5-methylcytosine, 5-hydroxymethylcytosine, and 5-formylcytosine in the genomic DNA of human CMSCs isolated from diabetic donors. Whole heart genomic DNA analysis reveale…

Male0301 basic medicinePhysiologyPopulationheartBiologyMixed Function OxygenasesCytosineMice03 medical and health sciencesProto-Oncogene ProteinsfibroblastsHuman Umbilical Vein Endothelial CellsAnimalsHumansMyocytes CardiacEpigeneticsEnzyme InhibitorseducationCells CulturedEpigenomicsDemethylationeducation.field_of_studyDNA methylationDNA methylation; epigenomics; fibroblasts; heart; hyperglycemia; metabolism; physiology; cardiology and cardiovascular medicineMesenchymal Stem CellsSettore MED/13 - ENDOCRINOLOGIABase excision repairMolecular biologyThymine DNA GlycosylaseMice Inbred C57BLHEK293 Cells030104 developmental biologyDNA demethylationDiabetes Mellitus Type 2epigenomicsDNA methylationKetoglutaric AcidshyperglycemiaThymine-DNA glycosylaseCardiology and Cardiovascular MedicineOxidation-ReductionmetabolismCirculation Research
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Myocardial maladaptation to pressure overload in CB2 receptor-deficient mice

2019

Abstract Background Adaptation to aortic valve stenosis leads to myocardial hypertrophy, which has been associated with inflammation, fibrosis and activation of the endocannabinoid system. Since the endocannabinoid system and the CB2 receptor provide cardioprotection and modulate immune response in experimental ischemia, we investigated the role of CB2 in a mouse model of cardiac pressure overload. Methods Transverse aortic constriction was performed in CB2 receptor-deficient (Cnr2−/−) mice and their wild-type littermates (Cnr2+/+). After echocardiography and Millar left heart catheter hemodynamic evaluation hearts were processed for histological, cellular and molecular analyses. Results Th…

Male0301 basic medicinemedicine.medical_specialtyGenotypeFluorescent Antibody TechniqueBlood PressureCardiomegalyInflammation030204 cardiovascular system & hematologyProinflammatory cytokineReceptor Cannabinoid CB2Mice03 medical and health sciences0302 clinical medicineImmune systemFibrosisInternal medicineVentricular DysfunctionmedicineAnimalsMyocytes CardiacMolecular BiologyMice KnockoutPressure overloadCardioprotectionVentricular RemodelingChemistryMyocardiumHemodynamicsmedicine.diseaseImmunohistochemistryEndocannabinoid systemDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyFemaleInflammation Mediatorsmedicine.symptomCardiology and Cardiovascular MedicineMyofibroblastBiomarkersEndocannabinoidsJournal of Molecular and Cellular Cardiology
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Investigating the Vascular Toxicity Outcomes of the Irreversible Proteasome Inhibitor Carfilzomib

2020

Background: Carfilzomib&rsquo

Male0301 basic medicinevasculature030204 cardiovascular system & hematologyPharmacologyDinoprostEndoplasmic Reticulumlcsh:ChemistryMicechemistry.chemical_compound0302 clinical medicineAMP-Activated Protein Kinase Kinasesvascular smooth muscle cellsCytotoxicitylcsh:QH301-705.5endoplasmatic-reticulum stressSpectroscopychemistry.chemical_classificationcarfilzomibCobaltGeneral MedicineMetforminComputer Science ApplicationsRespiratory burstMetforminDrug Therapy CombinationGlycolysisOligopeptidesProteasome Inhibitorsmedicine.drugProteasome Endopeptidase ComplexautophagyCell SurvivalMyocytes Smooth MuscleAntineoplastic AgentsNitric OxideArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyReactive oxygen speciesbusiness.industryOrganic ChemistryAutophagyCarfilzomibActinsVasoprotectiveMice Inbred C57BLGlucose030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999Proteasome inhibitorTumor Suppressor Protein p53Reactive Oxygen SpeciesbusinessProtein KinasesInternational Journal of Molecular Sciences
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Systemic blockade of ACVR2B ligands protects myocardium from acute ischemia-reperfusion injury

2019

Activin A and myostatin, members of the transforming growth factor (TGF)-β superfamily of secreted factors, are potent negative regulators of muscle growth, but their contribution to myocardial ischemia-reperfusion (IR) injury is not known. The aim of this study was to investigate if activin 2B (ACVR2B) receptor ligands contribute to myocardial IR injury. Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) and subjected to myocardial ischemia followed by reperfusion for 6 or 24 h. Systemic blockade of ACVR2B ligands by ACVR2B-Fc was protective against cardiac IR injury, as evidenced by reduced infarcted area, apoptosis, and autophagy and better preserved LV systolic function fo…

MaleActivin Receptors Type IIiskemialihaksetSmad2 ProteinMyostatinPharmacologyMice0302 clinical medicineDrug DiscoverykasvutekijätMyocytes CardiacCardioprotection0303 health sciences318 Medical biotechnologybiologysydänactivins1184 Genetics developmental biology physiologyII RECEPTORS3. Good health030220 oncology & carcinogenesisMolecular MedicineOriginal ArticleSignal TransductionCardiac function curvegrowth differentiation factorsProgrammed cell deathBLOCKINGischemia-reperfusion injuryIschemiaMyocardial Reperfusion InjuryMASSta311103 medical and health sciencesMYOSTATIN-KNOCKOUTCARDIOPROTECTIONGeneticsmedicineAnimalsMolecular Biologylihassolut030304 developmental biologyPharmacologySKELETAL-MUSCLE GROWTHbusiness.industryMyocardiumFOLLISTATINMyostatinmedicine.diseaseACVR2BMice Inbred C57BLACTIVIN-AGDF11GDF11biology.protein3111 BiomedicineproteiinitbusinessReperfusion injuryDIFFERENTIATION FACTOR 11ACVR2BTranscription Factors
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Immunohistochemical marker for Na+ CP type Vα (C-20) and heterozygous nonsense SCN5A mutation W822X in a sudden cardiac death induced by mild anaphyl…

2009

A sudden death likely due to mild anaphylactic reaction in a young man is described. Autoptic, histologic, immunohistochemical, and laboratory findings were strongly consistent with the diagnosis of a mild anaphylactic reaction. Genetic molecular analysis, performed on formalin-fixed, paraffin-embedded tissues, showed a mutation described as W822X in a family with electrocardiographic pattern typical of Brugada Syndrome. It results in a nonsense mutation generating a truncated form of the channel protein. The mutation is due to a point substitution of a guanine with an adenine residue (G2466A). Immunohistochemistry and laser scanning confocal microscopy on sections from heart formalin-fixed…

MaleChannellopathies; Confocal laser scanning microscopy; Immunohistochemistry; Na+ CP type Vα (C-20); Sodium channel; Sudden cardiac death; W822X; Adult; Anaphylaxis; Brugada Syndrome; Fatal Outcome; Humans; Male; Muscle Proteins; Myocardium; Myocytes Cardiac; NAV1.5 Voltage-Gated Sodium Channel; Peanut Hypersensitivity; Sodium Channels; Death Sudden Cardiac; Mutation Missense; 2734; Medical Laboratory Technology; HistologyMuscle Proteinsmedicine.disease_causeSodium ChannelsSudden cardiac deathNAV1.5 Voltage-Gated Sodium ChannelNa+ CP type V[alpha] (C-20)Fatal OutcomeMissense mutationMyocytes CardiacConfocal laser scanning microscopyCP type Vα (C-20)Cellular localizationBrugada syndromeBrugada SyndromeMutationChemistrySodium channelChannellopathiesImmunohistochemistryChannellopathies; Confocal laser scanning microscopy; Immunohistochemistry; Na; +; CP type Vα (C-20); Sodium channel; Sudden cardiac death; W822XDeathMedical Laboratory TechnologyCardiologyCardiacAdultmedicine.medical_specialtyHistologyNa+ CP type V[alpha] (C-20) confocal laser scanning microscopy immunohistochemistry sodium channel channellopathies W822X sudden cardiac deathNonsense mutation2734Mutation MissenseSocio-culturaleNa+ CP type Vα (C-20)+Sudden deathPathology and Forensic MedicineInternal medicinemedicineHumansPeanut HypersensitivityNacardiovascular diseasesW822XAnaphylaxisMyocytesSodium channelMyocardiummedicine.diseaseMolecular biologySuddenSudden cardiac deathDeath Sudden CardiacMutationMissenseNa+ CP type V[alpha] (C-20); confocal laser scanning microscopy; immunohistochemistry; sodium channel; channellopathies; W822X; sudden cardiac death
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A multicentre case control study on complicated coeliac disease: two different patterns of natural history, two different prognoses

2014

Background: Coeliac disease is a common enteropathy characterized by an increased mortality mainly due to its complications. The natural history of complicated coeliac disease is characterised by two different types of course: patients with a new diagnosis of coeliac disease that do not improve despite a strict gluten-free diet (type A cases) and previously diagnosed coeliac patients that initially improved on a gluten-free diet but then relapsed despite a strict diet (type B cases). Our aim was to study the prognosis and survival of A and B cases. Methods: Clinical and laboratory data from coeliac patients who later developed complications (A and B cases) and sex- and age-matched coeliac p…

MaleComplicationsSettore MED/09 - Medicina InternaLymphomaSmallGastroenterologyCoeliac diseaseEnteropathy-Associated T-Cell LymphomaIntestine SmallMedicineCeliac diseaseEnteropathyTreatment FailureINTESTINAL T-CELL LYMPHOMAGastroenterologyGLUTEN FREE DIETGeneral Medicinecomplicated coeliac disease; natural history; prognosis;IleitisMiddle AgedPrognosisEnteritisIntestineNatural historyAdult; Aged; Carcinoma; Case-Control Studies; Celiac Disease; Collagenous Sprue; Disease Progression; Enteritis; Enteropathy-Associated T-Cell Lymphoma; Female; Humans; Ileitis; Intestinal Neoplasms; Intestine Small; Jejunal Diseases; Lymphoma B-Cell; Male; Middle Aged; Prognosis; Treatment Failure; Diet Gluten-Freenatural historyGluten-free dietDisease ProgressionEnteropathy-associated T-cell lymphomaFemaleprognosiResearch ArticleCollagenous SprueAdultmedicine.medical_specialtyLymphoma B-CellGlutensSettore MED/12 - GASTROENTEROLOGIAcomplicated coeliac diseasecomplications/drug therapy/mortality Myocytes; celiac diseaseNODiet Gluten-FreeInternal medicineIntestinal NeoplasmsHumanscomplications/drug therapy/mortalitySurvival rateCELIAC DISEASE; Complications; INTESTINAL T-CELL LYMPHOMA; prognosis; GLUTEN FREE DIETAgedcomplications/drug therapy/mortality; Myocytes; celiac diseaseMyocytesbusiness.industryCarcinomaB-CellCase-control studynutritional and metabolic diseasesJejunal DiseasesHepatologymedicine.diseasedigestive system diseasesDietEATLCase-Control StudiesGluten-FreeGluten freebusinessComplicationcoeliac disease
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Single mechano-gated channels activated by mechanical deformation of acutely isolated cardiac fibroblasts from rats

2010

Aim Mechanosensitive conductances were reported in cardiac fibroblasts, but the properties of single channels mediating their mechanosensitivity remain uncharacterized. The aim of this work was to investigate single mechano-gated channels (MGCs) activated by mechanical deformations of cardiac fibroblasts. Methods Currents through single MGCs and mechanosensitive whole-cell currents were recorded from isolated rat atrial fibroblasts using the cell-attached and whole-cell patch-clamp configurations respectively. Defined mechanical stress was applied via the patch pipette used for the whole-cell recordings. Results Under resting conditions occasional short openings of two types of single MGCs …

MaleCytochalasin DPatch-Clamp TechniquesPhysiologyCell SeparationIon Channelschemistry.chemical_compoundPressureAnimalsMyocyteMyocytes CardiacHeart AtriaPatch clampReversal potentialCell ShapeNucleic Acid Synthesis InhibitorsCytochalasin DPipetteAnatomyFibroblastsElectric StimulationRatsElectrophysiologySolutionsCoupling (electronics)ElectrophysiologychemistryBiophysicsMechanosensitive channelsColchicineIon Channel GatingActa Physiologica
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