Search results for " Myocytes"

showing 10 items of 11 documents

Different muscarinic receptor subtypes modulate proliferation of primary human detrusor smooth muscle cells via Akt/PI3K and map kinases.

2013

While acetylcholine (ACh) and muscarinic receptors in the bladder are mainly known for their role in the regulation of smooth muscle contractility, in other tissues they are involved in tissue remodelling and promote cell growth and proliferation. In the present study we have used primary cultures of human detrusor smooth muscle cells (HDSMCs), in order to investigate the role of muscarinic receptors in HDSMC proliferation. Samples were obtained as discarded tissue from men >65 years undergoing radical cystectomy for bladder cancer and cut in pieces that were either immediately frozen or placed in culture medium for the cell culture establishment. HDSMCs were isolated from samples, propagat…

AtropineMalePyrrolidinesMessenger030232 urology & nephrologyGene ExpressionPhosphatidylinositol 3-Kinases0302 clinical medicineAged Atropine; pharmacology Benzofurans; pharmacology Carbachol; pharmacology Cell Proliferation Cells; Cultured Cholinergic Agonists; pharmacology Gene Expression Humans Male Mitogen-Activated Protein Kinases; metabolism Muscarinic Antagonists; pharmacology Myocytes; Smooth Muscle; metabolism Phosphatidylinositol 3-Kinases; metabolism Piperidines; pharmacology Pirenzepine; analogs /&/ derivatives/pharmacology Proto-Oncogene Proteins c-akt; metabolism Pyrrolidines; pharmacology RNA; Messenger; metabolism Receptors; Muscarinic; physiology Urinary Bladder; cytologyPiperidinesSmooth MuscleReceptorsMuscarinic acetylcholine receptor M5Muscarinic acetylcholine receptorCells CulturedCulturedMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2Smooth muscle contractionMuscarinic acetylcholine receptor M1Receptors Muscarinic030220 oncology & carcinogenesisMitogen-Activated Protein KinasesAcetylcholinemedicine.drugmedicine.medical_specialtyCarbacholCellsMyocytes Smooth MuscleUrinary BladderMuscarinic AntagonistsBiologyCholinergic Agonists03 medical and health sciencesInternal medicineMuscarinicmedicineHumansRNA MessengerAgedBenzofuransCell ProliferationPharmacologyMyocytesPirenzepineEndocrinologyphysiologycytologyRNACarbacholanalogs /&/ derivatives/pharmacologymetabolismProto-Oncogene Proteins c-aktPharmacological research
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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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Lysed Erythrocyte Membranes Promote Vascular Calcification

2019

Background: Intraplaque hemorrhage promotes atherosclerosis progression, and erythrocytes may contribute to this process. In this study we examined the effects of red blood cells on smooth muscle cell mineralization and vascular calcification and the possible mechanisms involved. Methods: Erythrocytes were isolated from human and murine whole blood. Intact and lysed erythrocytes and their membrane fraction or specific erythrocyte components were examined in vitro using diverse calcification assays, ex vivo by using the murine aortic ring calcification model, and in vivo after murine erythrocyte membrane injection into neointimal lesions of hypercholesterolemic apolipoprotein E–deficient mi…

0303 health sciencesLysisbusiness.industrySmooth muscle myocytes030204 cardiovascular system & hematologyCell biology03 medical and health sciences0302 clinical medicineMembraneSmooth musclePhysiology (medical)MedicineCardiology and Cardiovascular MedicinebusinessVascular calcificationProcess (anatomy)030304 developmental biologyCirculation
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Implication du récepteur 5-HT4 cardiaque humain dans la fibrillation auriculaire : rôle d’auto-anticorps dirigés contre ce récepteur ?

2004

The human cardiac 5-HT4 receptor was cloned in 1997. It is functional only in atrial myocytes where it is positively coupled via Gs to the adenylate cyclase, activates the cAMP-dependent protein kinase (PKA) and in consequence phosphorylates a variety of intracellular proteins implicated in excitation-contraction coupling. A number of studies suggest a role for the 5-HT4 receptor in the maintenance or elongation of atrial fibrillation. It is now accepted that certain cardiac pathologies involve auto-immune processes. Antibodies directed against the second extracellular loop of a number of cardiac G-protein linked receptors have been found. The human cardiac 5-HT4 receptor could therefore al…

human atrial myocytesantibodyreceptorfibrillation auriculaireanticorpssérotonineatrial fibrillation[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmyocytes atriaux humainsrécepteur[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemserotonin
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The Amino-Terminal Domain of GRK5 Inhibits Cardiac Hypertrophy through the Regulation of Calcium-Calmodulin Dependent Transcription Factors.

2018

We have recently demonstrated that the amino-terminal domain of G protein coupled receptor kinase (GRK) type 5, (GRK5-NT) inhibits NFκB activity in cardiac cells leading to a significant amelioration of LVH. Since GRK5-NT is known to bind calmodulin, this study aimed to evaluate the functional role of GRK5-NT in the regulation of calcium-calmodulin-dependent transcription factors. We found that the overexpression of GRK5-NT in cardiomyoblasts significantly reduced the activation and the nuclear translocation of NFAT and its cofactor GATA-4 in response to phenylephrine (PE). These results were confirmed in vivo in spontaneously hypertensive rats (SHR), in which intramyocardial adenovirus-med…

0301 basic medicineG-Protein-Coupled Receptor Kinase 5MalecalmodulinMutantWistarPlasma protein binding030204 cardiovascular system & hematologyCatalysilcsh:ChemistryPhenylephrine0302 clinical medicineRats Inbred SHRMyocytes Cardiaclcsh:QH301-705.5SpectroscopybiologyChemistrycardiac hypertrophyNFATComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineLeft VentricularComputer Science ApplicationsCell biologycardiac hypertrophy; transcription factors; calmodulin; GRKGRKHypertrophy Left VentricularCardiacProtein BindingInbred SHRCalmodulinCalmodulin; Cardiac hypertrophy; GRK; Transcription factors; Animals; Binding Sites; Calmodulin; Cell Line; G-Protein-Coupled Receptor Kinase 5; GATA4 Transcription Factor; Hypertrophy Left Ventricular; Male; Myocytes Cardiac; NFATC Transcription Factors; Phenylephrine; Protein Binding; Rats; Rats Inbred SHR; Rats Wistar; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryCatalysisArticleCell LineInorganic Chemistry03 medical and health sciencesG-Protein-Coupled Receptor Kinase 5transcription factorsAnimalsPhysical and Theoretical ChemistryRats WistarTranscription factorMolecular BiologyG protein-coupled receptor kinaseMyocytesBinding SitesNFATC Transcription FactorsOrganic ChemistryHypertrophyNFATC Transcription FactorsGATA4 Transcription FactorRats030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinTranscription factorInternational journal of molecular sciences
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Atrial natriuretic peptide and CD34 overexpression in human idiopathic dilated cardiomyopathies.

2007

Idiopathic dilated cardiomyopathy (IDCM) is a primary myocardial disease of unknown cause characterized by ventricular chamber enlargement with impaired contractile function. In familial forms of IDCM, mutations of genes coding for cytoskeletal proteins related to force transmission, such as dystrophin, cardiac actin, desmin, and delta-sarcoglycan, have been identified. Here, we report the data of a retrospective investigation carried out to evaluate the expression of atrial natriuretic peptide (ANP), CD34, troponin T and nestin in the myocardium of patients affected with IDCM. Formalin-fixed and paraffin-embedded consecutive tissue sections from the ventricular wall of 10 human normal hear…

Microbiology (medical)ventricular myocytesCardiomyopathy Dilatedmedicine.medical_specialtyHeart VentriclesCardiomyopathyAntigens CD34Nerve Tissue ProteinsANP; CD34; nestin; troponin T; endothelial cells; ventricular myocytesPathology and Forensic MedicineNestinAtrial natriuretic peptideIntermediate Filament ProteinsTroponin TAntigens CDReference ValuesInternal medicineIdiopathic dilated cardiomyopathymedicineImmunology and AllergyHumansTroponin Tbiologybusiness.industryDilated cardiomyopathyGeneral MedicineNestinmedicine.diseaseTroponinImmunohistochemistryCardiologybiology.proteinendothelial cellDesminCD34AutopsybusinessANPAtrial Natriuretic FactorBiomarkersAPMIS : acta pathologica, microbiologica, et immunologica Scandinavica
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Carbon monoxide improves cardiac energetics and safeguards the heart during reperfusion after cardiopulmonary bypass in pigs

2004

Ischemia-reperfusion injury, a clinical problem during cardiac surgery, involves worsened adenosine trisphosphate (ATP) generation and damage to the heart. We studied carbon monoxide ( CO) pretreatment, proven valuable in rodents but not previously tested in large animals, for its effects on pig hearts subjected to cardiopulmonary bypass with cardioplegic arrest. Hearts of CO-treated pigs showed significantly higher ATP and phosphocreatine levels, less interstitial edema, and apoptosis of cardiomyocytes and required fewer defibrillations after bypass. We conclude that treatment with CO improves the energy status, prevents edema formation and apoptosis, and facilitates recovery in a clinical…

Sus scrofaMyocardial IschemiaApoptosisCardiotonic AgentsBiochemistrylaw.inventionchemistry.chemical_compoundAdenosine Triphosphateischemia reperfusion; heart arrest; apoptosis; hypoxia; Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Animals; Apoptosis; Carbon Monoxide; Cardiotonic Agents; Edema; Electric Countershock; Energy Metabolism; Female; Guanosine Triphosphate; Heart; Myocardial Ischemia; Myocardial Reperfusion Injury; Myocytes Cardiac; NAD; NADP; Oxidation-Reduction; Sus scrofa; Cardiopulmonary BypasslawEdemaEdemaMyocytes CardiacCarbon MonoxideCardiopulmonary BypassMED/04 - PATOLOGIA GENERALEHeartCardiac surgeryAdenosine DiphosphateAnesthesiaCardiologyFemaleGuanosine Triphosphatemedicine.symptomCardiacOxidation-ReductionBiotechnologymedicine.drugischemia reperfusion; heart arrest; apoptosis; hypoxiaAdenosine monophosphatemedicine.medical_specialtyCardiotonic AgentsElectric CountershockMyocardial Reperfusion InjuryPhosphocreatineInternal medicineGeneticsmedicineCardiopulmonary bypassischemia reperfusionAnimalsMolecular BiologyMyocytesbusiness.industryhypoxiaNADAdenosineapoptosiAdenosine MonophosphateAdenosine diphosphatechemistryEnergy MetabolismbusinessNADPheart arrest
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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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Ranolazine-Mediated Attenuation of Mechanoelectric Feedback in Atrial Myocyte Monolayers.

2020

[EN] Background Mechanical stretch increases Na(+)inflow into myocytes, related to mechanisms including stretch-activated channels or Na+/H(+)exchanger activation, involving Ca(2+)increase that leads to changes in electrophysiological properties favoring arrhythmia induction. Ranolazine is an antianginal drug with confirmed beneficial effects against cardiac arrhythmias associated with the augmentation ofI(NaL)current and Ca(2+)overload. Objective This study investigates the effects of mechanical stretch on activation patterns in atrial cell monolayers and its pharmacological response to ranolazine. Methods Confluent HL-1 cells were cultured in silicone membrane plates and were stretched to…

0301 basic medicineMechanical stretchOptical mappingMechanoelectric feedbackPhysiologyRanolazine030204 cardiovascular system & hematologyFibrillatory patternslcsh:PhysiologyTECNOLOGIA ELECTRONICA03 medical and health sciences0302 clinical medicineRanolazinePhysiology (medical)Optical mappingMonolayermechanoelectric feedbackmedicineMyocyterotor dynamic analysisAtrial myocytesranolazineOriginal ResearchFibrillationHL-1 celllcsh:QP1-981ChemistryAttenuationmechanical stretchElectrophysiologyRotor dynamic analysisoptical mapping030104 developmental biologyfibrillatory patternsBiophysicsmedicine.symptommedicine.drugFrontiers in physiology
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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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