Search results for "Myoblasts"

showing 10 items of 26 documents

Expression of the rat connexin 39 (rCx39) gene in myoblasts and myotubes in developing and regenerating skeletal muscles: an in situ hybridization st…

2005

We report a detailed analysis of the expression pattern of the recently identified rat connexin gene, named rat connexin 39 (rCx39), both during embryonic development and in adult life. Qualitative and quantitative reverse transcription/polymerase chain reaction analysis showed intense expression of rCx39 restricted to differentiating skeletal muscles, with a peak of expression detected at 18 days of embryonic life, followed by a rapid decline to undetectable levels within the first week of postnatal life. A combination of the in situ hybridization technique for the detection of rCx39 mRNA and immunohistochemistry for myogenin, a myoblast-specific marker, allowed us to establish that the mR…

MaleHistologyTime FactorsGap junctionMyoblasts SkeletalMolecular Sequence DataMuscle Fibers SkeletalConnexinIn situ hybridizationBiologyConnexinsPathology and Forensic MedicineSatellite cellsmedicineMyocyteAnimalsCell LineageTissue DistributionAmino Acid SequenceRNA MessengerRats WistarMuscle SkeletalMyogeninIn Situ HybridizationPhylogenyMessenger RNABase SequenceSequence Homology Amino AcidMyogenesisReverse Transcriptase Polymerase Chain ReactionRegeneration (biology)Skeletal muscleGene Expression Regulation DevelopmentalCell BiologyMolecular biologyImmunohistochemistryProtein Structure TertiaryRatsmedicine.anatomical_structureMyogenesiMyogeninMyogenic cell lineageCell and tissue research
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Single-cell trajectories reconstruction, exploration and mapping of omics data with STREAM

2019

Single-cell transcriptomic assays have enabled the de novo reconstruction of lineage differentiation trajectories, along with the characterization of cellular heterogeneity and state transitions. Several methods have been developed for reconstructing developmental trajectories from single-cell transcriptomic data, but efforts on analyzing single-cell epigenomic data and on trajectory visualization remain limited. Here we present STREAM, an interactive pipeline capable of disentangling and visualizing complex branching trajectories from both single-cell transcriptomic and epigenomic data. We have tested STREAM on several synthetic and real datasets generated with different single-cell techno…

0301 basic medicineEpigenomicsMultifactor Dimensionality ReductionComputer scienceGeneral Physics and Astronomy02 engineering and technologyOmics dataMyoblastsMiceSingle-cell analysisGATA1 Transcription FactorMyeloid CellsLymphocyteslcsh:ScienceData processingMultidisciplinaryQGene Expression Regulation DevelopmentalRNA sequencingCell DifferentiationGenomics021001 nanoscience & nanotechnologyData processingDNA-Binding ProteinsInterferon Regulatory FactorsSingle-Cell Analysis0210 nano-technologyAlgorithmsOmics technologiesSignal TransductionLineage differentiationScienceComputational biologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesErythroid CellsAnimalsCell LineageGeneral Chemistrydevelopmental trajectories visualizationHematopoietic Stem CellsPipeline (software)Visualization030104 developmental biologyTheoryofComputation_MATHEMATICALLOGICANDFORMALLANGUAGESCellular heterogeneitySingle cell analysilcsh:QGene expressionTranscriptomeTranscription FactorsNature Communications
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Crude oil exposures reveal roles for intracellular calcium cycling in haddock craniofacial and cardiac development.

2016

AbstractRecent studies have shown that crude oil exposure affects cardiac development in fish by disrupting excitation-contraction (EC) coupling. We previously found that eggs of Atlantic haddock (Melanogrammus aeglefinus) bind dispersed oil droplets, potentially leading to more profound toxic effects from uptake of polycyclic aromatic hydrocarbons (PAHs). Using lower concentrations of dispersed crude oil (0.7–7 μg/L ∑PAH), here we exposed a broader range of developmental stages over both short and prolonged durations. We quantified effects on cardiac function and morphogenesis, characterized novel craniofacial defects, and examined the expression of genes encoding potential targets underly…

0301 basic medicineCardiac function curveFish ProteinsVDP::Mathematics and natural scienses: 400::Zoology and botany: 480::Marine biology: 497:Matematikk og naturvitenskap: 400::Kjemi: 440::Miljøkjemi naturmiljøkjemi: 446 [VDP]MorphogenesisIntracellular Space010501 environmental sciencesBiology:Mathematics and natural scienses: 400::Zoology and botany: 480::Marine biology: 497 [VDP]01 natural sciencesCalcium in biologyIon ChannelsArticleMyoblasts03 medical and health sciencesMorphogenesisVDP::Mathematics and natural scienses: 400::Chemistry: 440::Environmental chemistry natural environmental chemistry: 446AnimalsPetroleum PollutionCraniofacialPolycyclic Aromatic HydrocarbonsIon channel:Mathematics and natural scienses: 400::Chemistry: 440::Environmental chemistry natural environmental chemistry: 446 [VDP]Cells Cultured0105 earth and related environmental sciences:Matematikk og naturvitenskap: 400::Zoologiske og botaniske fag: 480::Marinbiologi: 497 [VDP]Calcium metabolismRegulation of gene expressionLife Cycle StagesMultidisciplinarySkullFishesGene Expression Regulation DevelopmentalHeartAnatomyEnvironmental ExposureCell biology030104 developmental biologyPetroleumVDP::Matematikk og naturvitenskap: 400::Zoologiske og botaniske fag: 480::Marinbiologi: 497VDP::Matematikk og naturvitenskap: 400::Kjemi: 440::Miljøkjemi naturmiljøkjemi: 446CalciumIntracellularScientific reports
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Comparative analysis of stress responses of H9c2 rat cardiomyoblasts following treatment with doxorubicin and tBOOH

2011

Abstract Cardiotoxicity is the major dose-limiting adverse effect of anthracyclines and is hypothesized to result from damage induced by reactive oxygen species (ROS) or inhibition of topoisomerase II. Here, we comparatively analyzed the effect of doxorubicin and the organic peroxide tertiary-butylhydroperoxide (tBOOH) on stress responses of rat cardiomyblast cells (H9c2). Moreover, we investigated the impact of serum factors and the novel prototypical protein kinase CK2 inhibitor resorufin on the sensentivity of H9c2 cells exposed to doxorubicin or tBOOH. Measuring cell viability by use of the WST assay as well as cell cycle progression and apoptotic death by FACS-based methods, we found t…

Programmed cell deathDNA damageCell SurvivalAntineoplastic AgentsApoptosisBiologyPharmacologyAntioxidantsCell Linetert-ButylhydroperoxidemedicineAnimalsDoxorubicinViability assayCytotoxicitychemistry.chemical_classificationReactive oxygen speciesCardiotoxicityDose-Response Relationship DrugKinaseCell BiologyMolecular biologyAcetylcysteineRatsOxidative StresschemistryDoxorubicinReactive Oxygen SpeciesMyoblasts Cardiacmedicine.drug
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Targeted therapy of liver fibrosis/cirrhosis and its complications.

2011

Department of Pharmacokinetics, Toxicology, and Targeting, University of Groningen, Antonius Deusinglaan 1, 9713 AV, Groningen, The Netherlands; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA; Division of Molecular and Translational Medicine, Johannes Gutenberg University, Langenbeckstr. 1, 55131 Mainz, Germany

Liver Cirrhosismedicine.medical_specialtyCirrhosisMacrophageKupffer CellsLiver fibrosismedicine.medical_treatmentKupffer cellTargeted therapyMyoblastsDrug Delivery SystemsInternal medicinemedicineHepatic Stellate CellsHumansHepatocyteMolecular Targeted TherapyHCCMyofibroblastTargetingDrug CarriersHepatologybusiness.industryGeneral surgeryAntifibrotic therapyMedical schoolTranslational medicineHepatologyFibroblastsmedicine.diseaseFibrosisLiverStellate cellHepatocytesDrugbusinessCholangiocyteJournal of hepatology
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Peroxisome proliferator-activated receptor δ (PPARδ) activation protects H9c2 cardiomyoblasts from oxidative stress-induced apoptosis

2005

Activation of peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARgamma plays beneficial roles in cardiovascular disorders such as atherosclerosis and heart reperfusion. Although PPARalpha and gamma have been documented to reduce oxidative stress in the vasculature and the heart, the role of PPARdelta remains poorly studied.We focused on PPARdelta function in the regulation of oxidative stress-induced apoptosis in the rat cardiomyoblast cell line H9c2. Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), we showed that PPARdelta is the predominantly expressed isotype whereas PPARalpha was weakly detected. By performing cell viability assays, we …

Programmed cell deathmedicine.medical_specialtyPhysiologyBlotting WesternPeroxisome proliferator-activated receptorApoptosisCaspase 3DNA FragmentationBiologyTransfectionmedicine.disease_causeCell LineGW501516Physiology (medical)Internal medicineIn Situ Nick-End LabelingmedicineAnimalsPPAR deltaViability assayReceptorchemistry.chemical_classificationCaspase 3Reverse Transcriptase Polymerase Chain ReactionHydrogen PeroxideCatalasemedicine.diseaseRatsUp-RegulationCell biologyOxidative StressThiazolesEndocrinologychemistryApoptosisCaspasesCardiology and Cardiovascular MedicineMyoblasts CardiacOxidative stressCardiovascular Research
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Aging-associated genes and let-7 microRNAs: a contribution to myogenic program dysregulation in oculopharyngeal muscular dystrophy

2019

Oculopharyngeal muscular dystrophy (OPMD) is a late-onset muscle disease caused by an abnormal (GCN) triplet expansion within the polyadenylate-binding protein nuclear 1 gene and consequent mRNA pr...

0301 basic medicineMaleAgingOculopharyngealMuscle DevelopmentBiochemistryMyoblasts0302 clinical medicine80 and overMuscular DystrophyHMGB1 ProteinPAX7 Transcription FactorCell DifferentiationdifferentiationMiddle AgedCell biologymedicine.anatomical_structureFemaleMyogeninMitogen-Activated Protein KinasesBiotechnologyDifferentiation regeneration skeletal muscleAdultBiologyInclusion BodyOculopharyngeal muscular dystrophy03 medical and health sciencesmicroRNAGeneticsmedicineHumansGenetic Predisposition to Diseasedifferentiation; regeneration; skeletal muscle; Adult; Aged; Aged 80 and over; Aging; Antigens Neoplasm; Cell Differentiation; Female; Gene Expression Regulation; HMGB1 Protein; Humans; Male; MicroRNAs; Middle Aged; Mitogen-Activated Protein Kinases; Muscle Development; Muscular Dystrophy Oculopharyngeal; Myoblasts; Myogenin; Myositis Inclusion Body; PAX7 Transcription Factor; Genetic Predisposition to Diseaseskeletal muscleAntigensMolecular BiologyGeneAgedMessenger RNAMyositisRegeneration (biology)Skeletal musclemedicine.diseaseMicroRNAs030104 developmental biologyMuscle diseaseGene Expression RegulationregenerationNeoplasm030217 neurology & neurosurgery
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Arsenic promotes NF-Κb-mediated fibroblast dysfunction and matrix remodeling to impair muscle stem cell function

2016

Abstract Arsenic is a global health hazard that impacts over 140 million individuals worldwide. Epidemiological studies reveal prominent muscle dysfunction and mobility declines following arsenic exposure; yet, mechanisms underlying such declines are unknown. The objective of this study was to test the novel hypothesis that arsenic drives a maladaptive fibroblast phenotype to promote pathogenic myomatrix remodeling and compromise the muscle stem (satellite) cell (MuSC) niche. Mice were exposed to environmentally relevant levels of arsenic in drinking water before receiving a local muscle injury. Arsenic-exposed muscles displayed pathogenic matrix remodeling, defective myofiber regeneration …

0301 basic medicineMyoblastSatellite Cells Skeletal MuscleCellSkeletal muscleBiologyMuscle DevelopmentArticleMyoblasts03 medical and health sciencesMiceStem CellmedicineAnimalsHumansMyocyteRegenerationFibroblastMuscle stem cellMyofibroblastMyogenesisAnimalStem CellsRegeneration (biology)arsenicNF-kappa BTranscription Factor RelASkeletal muscleGene Expression Regulation DevelopmentalCell BiologyFibroblastsCell biology030104 developmental biologymedicine.anatomical_structureMyogenesiImmunologyFibroblastMolecular MedicineStem cellMyofibroblastHumanSignal TransductionDevelopmental Biology
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Increased Muscleblind levels by chloroquine treatment improve myotonic dystrophy type 1 phenotypes in in vitro and in vivo models

2019

Myotonic dystrophy type 1 (DM1) is a life-threatening and chronically debilitating neuromuscular disease caused by the expansion of a CTG trinucleotide repeat in the 3′ UTR of the DMPK gene. The mutant RNA forms insoluble structures capable of sequestering RNA binding proteins of the Muscleblind-like (MBNL) family, which ultimately leads to phenotypes. In this work, we demonstrate that treatment with the antiautophagic drug chloroquine was sufficient to up-regulate MBNL1 and 2 proteins in Drosophila and mouse (HSA LR ) models and patient-derived myoblasts. Extra Muscleblind was functional at the molecular level and improved splicing events regulated by MBNLs in all disease models. In vivo,…

0301 basic medicinemusculoskeletal diseasesMaleRNA SplicingRNA-binding proteinBiologyMyotonic dystrophychloroquinemuscleblindMyoblasts03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineIn vivomedicineAutophagyMBNL1AnimalsDrosophila ProteinsHumansMyotonic DystrophytherapyMultidisciplinarymyotonic dystrophyMusclesRNANuclear ProteinsRNA-Binding ProteinsChloroquinemedicine.diseaseMyotoniaCell biologyDNA-Binding ProteinsDisease Models Animal030104 developmental biologyPhenotypechemistryPNAS PlusRNA splicingDrosophilaFemaleTrinucleotide repeat expansion030217 neurology & neurosurgery
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miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction

2014

Summary miR-133a and miR-1 are known as muscle-specific microRNAs that are involved in cardiac development and pathophysiology. We have shown that both miR-1 and miR-133a are early and progressively upregulated during in vitro cardiac differentiation of adult cardiac progenitor cells (CPCs), but only miR-133a expression was enhanced under in vitro oxidative stress. miR-1 was demonstrated to favor differentiation of CPCs, whereas miR-133a overexpression protected CPCs against cell death, targeting, among others, the proapoptotic genes Bim and Bmf. miR-133a-CPCs clearly improved cardiac function in a rat myocardial infarction model by reducing fibrosis and hypertrophy and increasing vasculari…

Cardiac function curveProgrammed cell deathMyocardial InfarctionGene ExpressionCardiomegalyBiologyBiochemistryArticleMuscle hypertrophyParacrine signallingDownregulation and upregulationmiR-133a; Cardiac Progenitors Cells; Myocardial InfarctionFibrosisREGENERATIONmicroRNAGeneticsmedicineMyocyteAnimalsRNA MessengerOXIDATIVE STRESSlcsh:QH301-705.5ENGINEERED HEART-TISSUElcsh:R5-920Gene Expression ProfilingMICRORNAComputational BiologyCell BiologyMUSCLEmedicine.disease3. Good healthCell biologyRatsAPOPTOSISHYPERTROPHYMicroRNAsDIFFERENTIATIONlcsh:Biology (General)ImmunologyGROWTHRNA Interferencelcsh:Medicine (General)EMBRYONIC STEM-CELLSMyoblasts CardiacDevelopmental BiologyStem Cell Reports
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