Search results for "Myocytes"

showing 10 items of 117 documents

The emerging role of miRNA-132/212 cluster in neurologic and cardiovascular diseases: Neuroprotective role in cells with prolonged longevity

2021

Abstract miRNA-132/212 are small regulators of gene expression with a function that fulfills a vital function in diverse biological processes including neuroprotection of cells with prolonged longevity in neurons and the cardiovascular system. In neurons, miRNA-132 appears to be essential for controlling differentiation, development, and neural functioning. Indeed, it also universally promotes axon evolution, nervous migration, plasticity as well, it is suggested to be neuroprotective against neurodegenerative diseases. Moreover, miRNA-132/212 disorder leads to neural developmental perturbation, and the development of degenerative disorders covering Alzheimer’s, Parkinson’s, and epilepsy’s …

Agingmedicine.medical_specialtyNeurologyDegenerative Disordermedia_common.quotation_subjectNeuroprotection03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmicroRNAAnimalsHumansMedicineMyocytes CardiacMolecular Targeted TherapyAxonCellular SenescenceComputingMilieux_MISCELLANEOUS030304 developmental biologymedia_commonNeurons0303 health sciencesbusiness.industryNeurodegenerationAutophagyLongevityNeurodegenerative Diseasesmedicine.diseaseNeuroprotection3. Good healthMicroRNAsmedicine.anatomical_structureGene Expression RegulationCardiovascular DiseasesbusinessNeuroscience030217 neurology & neurosurgeryDevelopmental Biology
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The transmembrane receptor Uncoordinated5 (Unc5) is essential for heart lumen formation in Drosophila melanogaster

2011

AbstractTransport of liquids or gases in biological tubes is fundamental for many physiological processes. Our knowledge on how tubular organs are formed during organogenesis and tissue remodeling has increased dramatically during the last decade. Studies on different animal systems have helped to unravel some of the molecular mechanisms underlying tubulogenesis. Tube architecture varies dramatically in different organs and different species, ranging from tubes formed by several cells constituting the cross section, tubes formed by single cells wrapping an internal luminal space or tubes that are formed within a cell. Some tubes display branching whereas others remain linear without interse…

AngiogenesisLumen (anatomy)Receptors Cell SurfaceOrganogenesisLumen formationBiologyLigandsUnc5AnimalsDrosophila ProteinsDrosophila heart morphogenesisMyocytes CardiacNerve Growth FactorsReceptorMolecular BiologyCardiogenesisTumor Suppressor ProteinsHeartCell BiologyAnatomyNetrin-1Tubulogenesisbiology.organism_classificationTransmembrane proteinCell biologyDrosophila melanogasterNetrinBSignal transductionDrosophila melanogasterNetrin ReceptorsDrosophila ProteinDevelopmental BiologyDevelopmental Biology
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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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Spontaneous Cardiomyocyte Differentiation From Adipose Tissue Stroma Cells

2004

Cardiomyocyte regeneration is limited in adult life. Thus, the identification of a putative source of cardiomyocyte progenitors is of great interest to provide a usable model in vitro and new perspective in regenerative therapy. As adipose tissues were recently demonstrated to contain pluripotent stem cells, the emergence of cardiomyocyte phenotype from adipose-derived cells was investigated. We demonstrated that rare beating cells with cardiomyocyte features could be identified after culture of adipose stroma cells without addition of 5-azacytidine. The cardiomyocyte phenotype was first identified by morphological observation, confirmed with expression of specific cardiac markers, immunocy…

AtropineMalemedicine.medical_specialtyStromal cellPhysiologyCellular differentiationHeart VentriclesCholinergic AgentsAdipose tissueAdipose tissueCardiomyocytes ; Adipose tissue ; Differentiation ; Stem cells ; Cell therapyStem cellsBiologyCell therapyCell therapyMiceAdrenergic Agents:CIENCIAS MÉDICAS ::Medicina interna [UNESCO]Internal medicinemedicineAnimalsMyocytes CardiacHeart AtriaProgenitor cellInduced pluripotent stem cellCells CulturedUNESCO::CIENCIAS MÉDICAS ::Medicina internaCardiomyocytesRegeneration (biology)Multipotent Stem CellsIsoproterenolCell Differentiation:CIENCIAS MÉDICAS [UNESCO]Myocardial ContractionPropranololCell biologyClone CellsMice Inbred C57BLEndocrinologyPhenotypeAdipose TissueDifferentiationUNESCO::CIENCIAS MÉDICASRNACarbacholStem cellStromal CellsCardiology and Cardiovascular MedicineMyoblasts Cardiac
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Biphasic Erk1/2 activation sequentially involving Gs and Gi signaling is required in beta3-adrenergic receptor-induced primary smooth muscle cell pro…

2013

Abstract The beta3 adrenergic receptor (B3-AR) reportedly induces cell proliferation, but the signaling pathways that were proposed, involving either Gs or Gi coupling, remain controversial. To further investigate the role of G protein coupling in B3-AR induced proliferation, we stimulated primary human myometrial smooth muscle cells with SAR150640 (B3-AR agonist) in the absence or presence of variable G-protein inhibitors. Specific B3-AR stimulation led to an Erk1/2 induced proliferation. We observed that the proliferative effects of B3-AR require two Erk1/2 activation peaks (the first after 3 min, the second at 8 h). Erk1/2 activation at 3 min was mimicked by forskolin (adenylyl-cyclase a…

Beta-3 adrenergic receptorGs alpha subunitMAP Kinase Signaling SystemMyocytes Smooth MuscleProliferationG protein coupled receptorBiologyGTP-Binding Protein alpha Subunits Gi-GoPertussis toxinchemistry.chemical_compoundErk1/2Protein kinasesCyclinsReceptors Adrenergic betaGTP-Binding Protein alpha Subunits GsHumansMolecular BiologyPI3K/AKT/mTOR pathwayCells CulturedG protein-coupled receptorCell ProliferationForskolinColforsinBeta-3 adrenergic receptorCell BiologyCell biologychemistryGene Expression RegulationPertussis ToxinMyometriumFemaleSignal transductionProto-oncogene tyrosine-protein kinase SrcBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Human stem cells from single blastomeres reveal pathways of embryonic or trophoblast fate specification.

2015

Mechanisms of initial cell fate decisions differ among species. To gain insights into lineage allocation in humans, we derived ten human embryonic stem cell lines (designated UCSFB1-10) from single blastomeres of four 8-cell embryos and one 12-cell embryo from a single couple. Compared with numerous conventional lines from blastocysts, they had unique gene expression and DNA methylation patterns that were, in part, indicative of trophoblast competence. At a transcriptional level, UCSFB lines from different embryos were often more closely related than those from the same embryo. As predicted by the transcriptomic data, immunolocalization of EOMES, T brachyury, GDF15 and active β-catenin reve…

BlastomeresTranscription GeneticCellular differentiationMedical and Health SciencesEmbryo Culture TechniquesEpigenomeNeural Stem CellsDevelopmentalMyocytes Cardiacbeta CateninOligonucleotide Array Sequence AnalysisEndodermGene Expression Regulation DevelopmentalEmbryoCell DifferentiationBiological SciencesStem Cells and RegenerationTrophoblastsmedicine.anatomical_structureembryonic structuresStem Cell Research - Nonembryonic - Non-HumanStem cellEndodermCardiacTranscriptionBrachyuryGrowth Differentiation Factor 151.1 Normal biological development and functioningBiologyCell LineGeneticUnderpinning researchmedicineGeneticsHumansHuman embryoCell LineageBlastocystMolecular BiologyEmbryonic Stem CellsMyocytesBlastomereHuman embryonic stem cellGene Expression ProfilingTrophoblastFibroblastsDNA MethylationStem Cell ResearchHuman trophoblast stem cellEmbryonic stem cellMolecular biology102Fate specificationBlastocystGene Expression RegulationGeneric health relevanceTranscriptomeDevelopmental Biology
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Gene Expression Analyses during Spontaneous Reversal of Cardiomyopathy in Mice with Repressed Nuclear CUG-BP, Elav-Like Family (CELF) Activity in Hea…

2015

CUG-BP, Elav-like family (CELF) proteins regulate cell type- and developmental stage-specific alternative splicing in the heart. Repression of CELF-mediated splicing activity via expression of a nuclear dominant negative CELF protein in heart muscle was previously shown to induce dysregulation of alternative splicing, cardiac dysfunction, cardiac hypertrophy, and dilated cardiomyopathy in MHC-CELFΔ transgenic mice. A “mild” line of MHC-CELFΔ mice that expresses a lower level of the dominant negative protein exhibits cardiac dysfunction and myopathy at a young age, but spontaneously recovers normal cardiac function and heart size with age despite the persistence of splicing defects. To the b…

CCAAT-Enhancer-Binding Protein-deltaMaleSerum Response FactorTranscription GeneticCardiomyopathylcsh:MedicineMice Transgenic030204 cardiovascular system & hematologyBiology03 medical and health sciencesMice0302 clinical medicineGene expressionSerum response factormedicineAnimalsHumansMyocytes Cardiaclcsh:Science030304 developmental biologyOligonucleotide Array Sequence AnalysisRegulation of gene expressionHemizygote0303 health sciencesMultidisciplinaryGene Expression ProfilingMyocardiumAlternative splicinglcsh:RGene targetingHeartmedicine.diseaseMolecular biologyCell biologyGene expression profilingAlternative SplicingGene Expression RegulationRNA splicinglcsh:QCalciumFemaleCardiomyopathiesResearch ArticlePLoS ONE
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Down-regulation of OPA1 alters mouse mitochondrial morphology, PTP function, and cardiac adaptation to pressure overload

2012

AIMS: The optic atrophy 1 (OPA1) protein is an essential protein involved in the fusion of the mitochondrial inner membrane. Despite its high level of expression, the role of OPA1 in the heart is largely unknown. We investigated the role of this protein in Opa1(+/-) mice, having a 50% reduction in OPA1 protein expression in cardiac tissue. METHODS AND RESULTS: In mutant mice, cardiac function assessed by echocardiography was not significantly different from that of the Opa1(+/+). Electron and fluorescence microscopy revealed altered morphology of the Opa1(+/-) mice mitochondrial network; unexpectedly, mitochondria were larger with the presence of clusters of fused mitochondria and altered c…

Cardiac function curveendocrine systemPhysiologyAdaptation BiologicalDown-RegulationBiologyMitochondrionMitochondrial Membrane Transport ProteinsPermeabilityGTP PhosphohydrolasesMitochondrial ProteinsMice03 medical and health sciencesMitochondrial membrane transport protein0302 clinical medicinePhysiology (medical)Optic Atrophy Autosomal DominantPressuremedicineAnimalsMyocyteMyocytes CardiacInner mitochondrial membrane030304 developmental biologyMice KnockoutPressure overload0303 health sciencesMitochondrial Permeability Transition Poremedicine.diseaseeye diseasesMitochondriaCell biologyBiochemistryMitochondrial permeability transition poreMitochondrial Membranesbiology.proteinOptic Atrophy 1Cardiology and Cardiovascular Medicine030217 neurology & neurosurgeryCardiovascular Research
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Inhibition of class I histone deacetylase with an apicidin derivative prevents cardiac hypertrophy and failure

2008

AIMS: Recent studies have demonstrated the importance of chromatin remodelling via histone acetylation/deacetylation for the control of cardiac gene expression. Specific histone deacetylases (HDACs) can, in fact, play a positive or negative role in determining cardiac myocyte (CM) size. Here, we report on the effect on hypertrophy development of three inhibitors (HDACi) of class I HDACs. METHODS AND RESULTS: The compounds were first analysed in vitro by scoring hypertrophy, expression of foetal genes, and apoptosis of neonatal rat CMs stimulated with phenylephrine, an alpha1-adrenergic agonist. This initial screening indicated that a truncated derivative of apicidin with class I HDAC specif…

Cardiac function curvemedicine.medical_specialtyHypertrophy Heart failurePhysiologymedicine.drug_classBiologyPeptides CyclicHistone DeacetylasesCell LineMuscle hypertrophychemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineAnimalsHumansMyocytes CardiacEnzyme InhibitorsRats WistarCells CulturedHeart FailurePressure overloadHistone deacetylase inhibitorHypertrophic cardiomyopathyHypertrophymedicine.diseaseRatsHistone Deacetylase InhibitorsDisease Models AnimalEndocrinologychemistryEchocardiographyHeart failureHypertrophy Left VentricularHistone deacetylaseCardiology and Cardiovascular MedicineApicidinCardiovascular Research
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Deleting Full Length Titin Versus the Titin M-Band Region Leads to Differential Mechanosignaling and Cardiac Phenotypes

2019

Background: Titin is a giant elastic protein that spans the half-sarcomere from Z-disk to M-band. It acts as a molecular spring and mechanosensor and has been linked to striated muscle disease. The pathways that govern titin-dependent cardiac growth and contribute to disease are diverse and difficult to dissect. Methods: To study titin deficiency versus dysfunction, the authors generated and compared striated muscle specific knockouts (KOs) with progressive postnatal loss of the complete titin protein by removing exon 2 (E2-KO) or an M-band truncation that eliminates proper sarcomeric integration, but retains all other functional domains (M-band exon 1/2 [M1/2]-KO). The authors evaluated c…

Cardiomyopathy DilatedMaleSarcomeresanimal structuresVentricular Dysfunction Rightmacromolecular substances030204 cardiovascular system & hematologyMechanotransduction CellularVentricular Function LeftArticleMuscle hypertrophyVentricular Dysfunction Left03 medical and health sciences0302 clinical medicinePhysiology (medical)AnimalsMedicineMyocytes CardiacMuscle Skeletal030304 developmental biologyMice Knockout0303 health sciencesbiologybusiness.industryMolecular springmusculoskeletal systemPhenotypeCell biologyMuscular AtrophyPhenotypeMuscle diseasecardiovascular systemVentricular Function Rightbiology.proteinTitinCardiology and Cardiovascular MedicinebusinessProtein KinasesGene DeletionDifferential (mathematics)Circulation
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