Search results for "Myocyte"

showing 10 items of 248 documents

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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Cardiac regenerative capacity is age- and disease-dependent in childhood heart disease

2018

Objective We sought to define the intrinsic stem cell capacity in pediatric heart lesions, and the effects of diagnosis and of age, in order to inform evidence-based use of potential autologous stem cell sources for regenerative medicine therapy. Methods Ventricular explants derived from patients with hypoplastic left heart syndrome (HLHS), tetralogy of Fallot (TF), dilated cardiomyopathy (DCM) and ventricular septal defect (VSD) were analyzed following standard in vitro culture conditions, which yielded cardiospheres (C-spheres), indicative of endogenous stem cell capacity. C-sphere counts generated per 5 mm3 tissue explant and the presence of cardiac progenitor cells were correlated to pa…

0301 basic medicineHeart Septal Defects VentricularAgingHeart diseaseCell TransplantationCardiovascular Proceduresmedicine.medical_treatmentCardiomyopathylcsh:Medicine030204 cardiovascular system & hematologyBiochemistryHypoplastic left heart syndromeTissue Culture TechniquesElectrocardiography0302 clinical medicineAnimal CellsHeart RegenerationHypoplastic Left Heart SyndromeNeurobiology of Disease and RegenerationMedicine and Health SciencesMorphogenesisBlood and Lymphatic System ProceduresMyocytes CardiacChildlcsh:ScienceCells CulturedTetralogy of FallotMultidisciplinaryStem CellsStem Cell TherapyDilated cardiomyopathyHeartStem-cell therapyCardiac Transplantationmedicine.anatomical_structureNeurologyChild PreschoolCardiologyTetralogy of Fallotcardiovascular systemStem cellCellular TypesAnatomyResearch ArticleCardiomyopathy Dilatedmedicine.medical_specialtyAdolescentHeart VentriclesSurgical and Invasive Medical Procedures03 medical and health sciencesInternal medicinemedicineHumansRegenerationVimentincardiovascular diseasesClinical GeneticsTransplantationbusiness.industrylcsh:RInfant NewbornCorrectionInfantBiology and Life SciencesProteinsMesenchymal Stem CellsCell BiologyOrgan Transplantationmedicine.diseaseCytoskeletal Proteins030104 developmental biologyVentricleCardiovascular Anatomylcsh:QbusinessOrganism DevelopmentDevelopmental BiologyStem Cell TransplantationPLoS ONE
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Considerations for an in vitro, cell-based testing platform for detection of adverse drug-induced inotropic effects in early drug development. Part 1…

2019

Drug-induced effects on cardiac contractility can be assessed through the measurement of the maximal rate of pressure increase in the left ventricle (LVdP/dtmax) in conscious animals, and such studies are often conducted at the late stage of preclinical drug development. Detection of such effects earlier in drug research using simpler, in vitro test systems would be a valuable addition to our strategies for identifying the best possible drug development candidates. Thus, testing platforms with reasonably high throughput, and affordable costs would be helpful for early screening purposes. There may also be utility for testing platforms that provide mechanistic information about how a given d…

0301 basic medicineInotropeDrugIn vitro testComputer sciencemedia_common.quotation_subjectcardiomyocyteReviewCardiomyocyteStem cellsContractilityInotropic statecontractilityContractility03 medical and health sciences0302 clinical medicinestem cellsmyocardiumPharmacology (medical)media_commoninotropic statePharmacologyMyocardiumlcsh:RM1-950Pre-clinical development030104 developmental biologylcsh:Therapeutics. PharmacologyDrug developmentRisk analysis (engineering)030220 oncology & carcinogenesisPressure increaseCell based
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Berberine Mediated Positive Inotropic Effects on Rat Hearts via a Ca2+-Dependent Mechanism

2020

Previous studies showed that berberine, an alkaloid from Coptis Chinensis Franch, might exert a positive inotropic effect on the heart. However, the underlying mechanisms were unclear. Here, we reported that berberine at 10-20 µM increased the left ventricular (LV) developed pressure and the maximal rate of the pressure rising, and it increased the maximal rate of the pressure descending at 20 µM in Langendorff-perfused isolated rat hearts. These effects diminished with the concentration of berberine increasing to 50 µM. In the concentration range of 50-300 µM, berberine increased the isometric tension of isolated left ventricular muscle (LVM) strips with or without electrical stimulations,…

0301 basic medicineInotropeheartPharmacology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBerberineNifedipineberberineExtracellularmedicineMyocytePharmacology (medical)positive inotropic effectPharmacologybiologyAlkaloidlcsh:RM1-950Coptis chinensisNa+biology.organism_classificationCa2+030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisIntracellularmedicine.drugFrontiers in Pharmacology
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Macrophage-induced reactive oxygen species promote myometrial contraction and labor-associated mechanisms

2020

AbstractAt labor, the myometrium is infiltrated by a massive influx of macrophages that secrete high levels of pro-inflammatory cytokines inducing the expression of specific labor-associated markers. However, the interactions between myocytes and macrophages and the role of macrophages in the myometrium at labor remain to be elucidated. In this work, we studied the role of myometrium-infiltrated macrophages and their interaction with myocytes in lipopolysaccharide-induced preterm labor. A co-culture model of human primary myometrial cells and macrophages was developed and validated. Collagen lattices were used to evaluate myocyte contraction. Differentiation steps were assessed by (i) phall…

0301 basic medicineLipopolysaccharideslabormacrophage03 medical and health scienceschemistry.chemical_compoundTransactivationUterine Contraction0302 clinical medicineMyocyteHumansoxidative stress[SDV.BDD]Life Sciences [q-bio]/Development BiologyCells Culturedmyocytechemistry.chemical_classificationReactive oxygen speciescell culture030219 obstetrics & reproductive medicinebiologySuperoxideMacrophagesMyometriumGap junctionParturitionCell DifferentiationCell BiologyGeneral MedicineHydrogen PeroxidedifferentiationVinculinCoculture TechniquesCell biology030104 developmental biologyReproductive Medicinechemistrybiology.proteinMyometriumFemaleSignal transductionReactive Oxygen Species
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Regulation of PDE5 expression in human aorta and thoracic aortic aneurysms

2019

AbstractAneurysms and dissections affecting thoracic aorta are associated with smooth muscle cell (SMC) dysfunction. NO/cGMP signaling pathway in smooth muscle cells has been shown to be affected in sporadic thoracic aortic aneurysms. We analyzed the mRNA levels of PDE5, a cGMP-hydrolyzing enzyme highly expressed in aortic SMCs, that regulates arterious vascular tone by lowering cGMP levels. We found that aortic tissue obtained from Marfan, tricuspid and bicuspid thoracic aneurysms expressed lower levels of PDE5 mRNA compared to control aortas. In particular, we found that affected aortas showed lower levels of all the PDE5A isoforms, compared to control aortas. Transfection of vascular SMC…

0301 basic medicineMaleCelllcsh:MedicineStimulationMuscle Smooth VascularAortic aneurysmchemistry.chemical_compound0302 clinical medicinePDE5 expression human aorta and thoracic aortic aneurysmsMyocyteThoracic aortalcsh:ScienceSettore BIO/16MultidisciplinaryTransfectionMiddle AgedIsoenzymesmedicine.anatomical_structurecardiovascular systemFemaleGene isoformAdultmedicine.medical_specialtyMyocytes Smooth MuscleArticleGene Expression Regulation EnzymologicNitric oxide03 medical and health sciencesmedicine.arteryInternal medicinemedicineHumansSettore MED/05 - Patologia ClinicaAgedCyclic Nucleotide Phosphodiesterases Type 5Aortic Aneurysm Thoracicbusiness.industrylcsh:Rmedicine.disease030104 developmental biologyEndocrinologychemistryRisk factorsthoracic aortic aneurysmslcsh:QAngiogenesisPDE5business030217 neurology & neurosurgery
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Levosimendan prevents doxorubicin-induced cardiotoxicity in time- and dose-dependent manner: implications for inotropy.

2019

Abstract Aims Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxi…

0301 basic medicineMaleMice 129 StrainTime FactorsHeart DiseasesNitric Oxide Synthase Type IIIPhysiology030204 cardiovascular system & hematologyPharmacology03 medical and health sciences0302 clinical medicineEnosPhysiology (medical)medicineCyclic AMPCyclic GMP-Dependent Protein KinasesAnimalsDoxorubicinMyocytes CardiacCalcium SignalingRats WistarProtein kinase BCyclic GMPCells CulturedSimendanCardioprotectionMice KnockoutCardiotoxicityAntibiotics AntineoplasticbiologyDose-Response Relationship DrugChemistryCalcium-Binding ProteinsMammary Neoplasms ExperimentalCardiovascular AgentsLevosimendanbiology.organism_classificationCyclic AMP-Dependent Protein KinasesMyocardial ContractionCardiotoxicityPhospholambanMice Inbred C57BL030104 developmental biologyDoxorubicinMilrinoneFemaleCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktmedicine.drugCardiovascular research
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Skeletal muscle Heat shock protein 60 increases after endurance training and induces peroxisome proliferator-activated receptor gamma coactivator 1 α…

2016

AbstractHeat shock protein 60 (Hsp60) is a chaperone localizing in skeletal muscle mitochondria, whose role is poorly understood. In the present study, the levels of Hsp60 in fibres of the entire posterior group of hindlimb muscles (gastrocnemius, soleus and plantaris) were evaluated in mice after completing a 6-week endurance training program. The correlation between Hsp60 levels and the expression of four isoforms of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α) were investigated only in soleus. Short-term overexpression of hsp60, achieved by in vitro plasmid transfection, was then performed to determine whether this chaperone could have a role in the activa…

0301 basic medicineMaleTime FactorsPPARgammaPeroxisome proliferator-activated receptorExosomesMiceendurance trainingMyocytechemistry.chemical_classificationMultidisciplinarytrainingbiologyHsp60Mitochondriamedicine.anatomical_structureMuscle Fibers Slow-TwitchMuscle Fibers Fast-TwitchHsp60; skeletal muscle; training; PPARgamma; PGC1αHSP60[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Oxidation-Reductionmedicine.medical_specialtyanimal structureschemical and pharmacologic phenomenacomplex mixturescachexiaArticleCell Line03 medical and health sciencesEndurance trainingHeat shock proteinInternal medicinePhysical Conditioning AnimalPGC1αCoactivatormedicineAnimals[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]skeletal muscleMuscle SkeletalSettore BIO/16 - Anatomia UmanafungiSkeletal muscleChaperonin 60030104 developmental biologyEndocrinologychemistryGene Expression RegulationChaperone (protein)biology.proteinPhysical EnduranceBiomarkersTranscription FactorsScientific Reports
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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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Physiological and Molecular Adaptations to Strength Training

2018

High muscle contraction forces that lead to gains in muscle function, size, and strength characterize resistance exercise training. The purpose of this chapter is to outline the adaptations in myofiber size and metabolism that occur by stimuli of hormones and local growth factors, mechanical and metabolic stress of muscle tissue, and myofibrillar disruptions induced by a resistance exercise bout. The chapter will highlight the network of intracellular pathways (including mTOR signaling) that ultimately lead to increases in gene expression and protein synthesis. Accumulation of acute exercise responses by systematic training over time modulate the muscle proteome that can be observed as chan…

0301 basic medicineMuscle tissueStrength trainingSkeletal muscle030229 sport sciencesBiologyMuscle hypertrophyCell biology03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structuremedicineMyocyteSignal transductionmedicine.symptomMyofibrilMuscle contraction
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