Search results for "Myoblasts"

showing 10 items of 26 documents

The cell-specific expression of metalloproteinase-disintegrins (ADAMs) in inflammatory myopathies

2007

Inflammatory cell invasion and cytokine activation are important steps in the pathogenesis of immune-mediated diseases of muscle. Metalloproteinase-disintegrins (ADAMs) are considered to play a critical role in leukocyte migration by promoting cellular adhesion, cleavage of molecules of the extracellular matrix and shedding of membrane bound cytokines. Here, we report the expression patterns of ADAM8, ADAM9, ADAM10, ADAM12, ADAM17 and ADAM19 in cultured human myoblasts and peripheral blood mononuclear cells (PBMCs) in vitro, as well as in biopsies from patients suffering from polymyositis (PM), dermatomyositis (DM), inclusion body myositis (IBM) and non-inflammatory controls. We observed an…

AdultMaleLeukocyte migrationBiopsyMyoblasts SkeletalMuscle Fibers SkeletalImmunologyT lymphocytesDown-RegulationGene ExpressionBiologyPeripheral blood mononuclear cellADAM19lcsh:RC321-571Downregulation and upregulationAutoimmune diseasemedicineHumansMyocytelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCells CulturedAgedMyositisMacrophagesMiddle Agedmedicine.diseaseMolecular biologyADAM ProteinsMatrix metalloproteinasesNeurologyImmunologyFemaleInflammation MediatorsInclusion body myositisADAM9ADAM8Neurobiology of Disease
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Protection by extra virgin olive oil against oxidative stress in vitro and in vivo. Chemical and biological studies on the health benefits due to a m…

2017

Abstract We report the results of in vivo studies in Caenorhabditis elegans nematodes in which addition of extra virgin olive oil (EVOO) to their diet significantly increased their life span with respect to the control group. Furthermore, when nematodes were exposed to the pesticide paraquat, they started to die after two days, but after the addition of EVOO to their diet, both survival percentage and lifespans of paraquat-exposed nematodes increased. Since paraquat is associated with superoxide radical production, a test for scavenging this radical was performed using cyclovoltammetry and the EVOO efficiently scavenged the superoxide. Thus, a linear correlation (y = -0.0838x +19.73, regres…

Animals; Caenorhabditis elegans; Cell Cycle; Cell Line; Electron Spin Resonance Spectroscopy; Humans; In Vitro Techniques; Olive Oil; Oxidative Stress; Paraquat; Rats; Reactive Oxygen Species; Diet Mediterranean0301 basic medicineAntioxidantmedicine.medical_treatmentlcsh:MedicineMediterraneanmedicine.disease_causeDiet MediterraneanBiochemistryAntioxidantsMonocytesMyoblastschemistry.chemical_compoundWhite Blood Cells0302 clinical medicineParaquatGalvinoxylSuperoxidesAnimal CellsPlant ProductsMedicine and Health SciencesElectrochemistryFood sciencelcsh:Sciencechemistry.chemical_classificationMultidisciplinarySuperoxideStem CellsCell CycleAgricultureOxidesLipidsPeroxidesHydroperoxideChemistry030220 oncology & carcinogenesisPhysical SciencesCellular TypesResearch ArticleParaquatImmune CellsImmunologyIn Vitro TechniquesSettore BIO/09Vegetable OilsCell Line03 medical and health sciencesmedicineAnimalsHumansSettore BIO/10Caenorhabditis elegansOlive OilReactive oxygen speciesBlood CellsElectrode Potentialslcsh:RElectron Spin Resonance SpectroscopyChemical CompoundsBiology and Life SciencesCell BiologyAgronomyDietRatsTyrosolOxidative Stress030104 developmental biologychemistryHydroxytyrosollcsh:QReactive Oxygen SpeciesOilsOxidative stressCrop Science
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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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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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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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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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Control of apterous by vestigial drives indirect flight muscle development in drosophila

2003

0012-1606 (Print) Journal Article Research Support, Non-U.S. Gov't; Drosophila thoracic muscles are comprised of both direct flight muscles (DFMs) and indirect flight muscles (IFMs). The IFMs can be further subdivided into dorsolongitudinal muscles (DLMs) and dorsoventral muscles (DVMs). The correct patterning of each category of muscles requires the coordination of specific executive regulatory programs. DFM development requires key regulatory genes such as cut (ct) and apterous (ap), whereas IFM development requires vestigial (vg). Using a new vg(null) mutant, we report that a total absence of vg leads to DLM degeneration through an apoptotic process and to a total absence of DVMs in the …

MaleNerve Tissue Proteins/genetics/metabolismMuscle Fibers SkeletalMutantTranscription Factors/genetics/*metabolismmedicine.disease_causeMyoblastsTwist transcription factorMyoblasts/physiologyDrosophila ProteinsWings AnimalDevelopmentalCells CulturedRegulator geneRegulation of gene expressionWing/growth & development/physiologyMutationCulturedMusclesGene Expression Regulation DevelopmentalNuclear ProteinsDrosophila Proteins/genetics/*metabolismAnatomyMuscle degenerationCell biologytwistDrosophilacutMuscles/metabolism/pathology/*physiologyIndirect flight musclesCellsLIM-Homeodomain ProteinsMuscle Fibers/pathology/physiologyNerve Tissue ProteinsBiologyvestigialNuclear Proteins/genetics/*metabolismmedicineHomeodomain Proteins/genetics/*metabolismAnimalsDrosophila/*growth & developmentDrosophilaMolecular BiologyHomeodomain ProteinsTwist-Related Protein 1Cell Biologybiology.organism_classificationapterousTwist Transcription FactorGene Expression RegulationMutationEctopic expressionTranscription FactorsDevelopmental BiologyDevelopmental Biology
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Regeneration of lingual musculature in rats using myoblasts over porcine bladder acellular matrix

2020

To use tissue engineering muscle repair (TEMR) for regenerating the lingual musculature of hemiglossectomized rats using neonatal myoblasts (NM) on porcine acellular urinary bladder matrix (AUBM).The study used 80 male rats. A volumetric muscle loss (VML) injury was created on the left side of the tongue. The rats were randomized into four groups: Group 1 (AUBM + myoblasts); Group 2 (AUBM); Group 3 (myoblasts); and Group 4 (control). NM were obtained from neonatal rats. The animals were weighed on day 0 and just before euthanasia. Five rats in each group were euthanized at days 2, 14, 28, and 42; the tongues were prepared for morphometric analysis, postoperative left hemitongue weight, and …

MaleSwineUrinary BladderMatrix (biology)Myoblasts03 medical and health sciences0302 clinical medicineTongueTissue engineeringTonguemedicineAnimalsRegenerationMyocyteGeneral DentistryUrinary bladderTissue Engineeringbusiness.industryRegeneration (biology)030206 dentistryAnatomymusculoskeletal systemRatsmedicine.anatomical_structureOtorhinolaryngology030220 oncology & carcinogenesisImmunohistochemistryDesminbusinessOral Diseases
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HACD1, a regulator of membrane composition and fluidity, promotes myoblast fusion and skeletal muscle growth

2015

International audience; The reduced diameter of skeletal myofibres is a hallmark of several congenital myopathies, yet the underlying cellular and molecular mechanisms remain elusive. In this study, we investigate the role of HACD1/PTPLA, which is involved in the elongation of the very long chain fatty acids, in muscle fibre formation. In humans and dogs, HACD1 deficiency leads to a congenital myopathy with fibre size disproportion associated with a generalized muscle weakness. Through analysis of HACD1-deficient Labradors, Hacd1-knockout mice, and Hacd1-deficient myoblasts, we provide evidence that HACD1 promotes myoblast fusion during muscle development and regeneration. We further demons…

Male[SPI.GPROC] Engineering Sciences [physics]/Chemical and Process EngineeringCellular differentiationGeneralized muscle weaknessBiologyMuscle Developmentcentronuclear myopathyCell LineMyoblasts03 medical and health scienceschemistry.chemical_compoundMyoblast fusionMice0302 clinical medicineDogsVLCFA[SDV.IDA]Life Sciences [q-bio]/Food engineeringGeneticsmedicineMyocyteAnimalsHumans[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringMUFACentronuclear myopathyMuscle SkeletalMolecular Biology030304 developmental biologyMice Knockout0303 health sciencesPTPLACell MembraneSkeletal muscleCell DifferentiationCell BiologyGeneral MedicineArticles[SDV.IDA] Life Sciences [q-bio]/Food engineeringmedicine.diseaseCongenital myopathyLysophosphatidylcholinemedicine.anatomical_structureLPCchemistryBiochemistryFemaleProtein Tyrosine Phosphatasescentronuclear myopathy;lpc;mufa;ptpla;vlcfa030217 neurology & neurosurgery
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Differentiation of Murine C2C12 Myoblasts Strongly Reduces the Effects of Myostatin on Intracellular Signaling

2020

Alongside in vivo models, a simpler and more mechanistic approach is required to study the effects of myostatin on skeletal muscle because myostatin is an important negative regulator of muscle size. In this study, myostatin was administered to murine (C2C12) and human (CHQ) myoblasts and myotubes. Canonical and noncanonical signaling downstream to myostatin, related ligands, and their receptor were analyzed. The effects of tumorkines were analyzed after coculture of C2C12 and colon cancer-C26 cells. The effects of myostatin on canonical and noncanonical signaling were strongly reduced in C2C12 cells after differentiation. This may be explained by increased follistatin, an endogenous blocke…

Muscle Fibers Skeletallcsh:QR1-502lihaksetlcsh:MicrobiologyArticleTGF-BETA SUPERFAMILYCell LineMyoblastsMicetumorkineCell Line TumorfollistatinAnimalsHumansCANCER CACHEXIAskeletal muscleMUSCLE ATROPHYlihassolutSmadsoluviestintäRECEPTORCell DifferentiationIN-VITROMyostatinmusculoskeletal systemMAPKActivinsLEUKEMIA INHIBITORY FACTORACTIVIN-AinflammationCulture Media ConditionedCELLSPROTEIN-SYNTHESISmyotubeGROWTH1182 Biochemistry cell and molecular biologyproteiinit3111 BiomedicinecocultureSignal Transduction
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