Search results for "Myocyte"

showing 10 items of 248 documents

Intramuscular Extracellular Matrix: Complex Environment of Muscle Cells

2002

KOVANEN, V. Intramuscular extracellular matrix: Complex environment of muscle cells. Exerc. Sport Sci. Rev., Vol. 30, No. 1, pp 20–25, 2002. Different collagen types among other extracellular matrix molecules, remodeling of the extracellular matrix with the aid of matrix metalloproteinases, and inte

IntegrinsChemistryFibrillar CollagensPhysical Therapy Sports Therapy and RehabilitationNon-Fibrillar CollagensExtracellular matrix moleculesMatrix metalloproteinaseBasement MembraneMatrix MetalloproteinasesExtracellular MatrixCell biologyExtracellular matrixHumansMyocyteOrthopedics and Sports MedicineMuscle SkeletalExercise and Sport Sciences Reviews
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Dystroglycan in Skin and Cutaneous Cells: β-Subunit Is Shed from the Cell Surface

2004

In skin, hemidesmosomal protein complexes attach the epidermis to the dermis and are critical for stable connection of the basal epithelial cell cytoskeleton with the basement membrane (BM). In muscle, a similar supramolecular aggregate, the dystrophin glycoprotein complex links the inside of muscle cells with the BM. A component of the muscle complex, dystroglycan (DG), also occurs in epithelia. In this study, we characterized the expression and biochemical properties of authentic and recombinant DG in human skin and cutaneous cells in vitro. We show that DG is present at the epidermal BM zone, and it is produced by both keratinocytes and fibroblasts in vitro. The biosynthetic precursor is…

KeratinocytesCellHuman skinPerlecanDermatologyTransfectionBiochemistryCell LineDystroglycanmedicineExtracellularMyocyteHumansCytoskeletonDystroglycansMolecular BiologyBasement membraneMembrane GlycoproteinsbiologyMembrane ProteinsDermisCell BiologyCell biologyCulture MediaProtein Structure TertiaryCytoskeletal Proteinsmedicine.anatomical_structureBiochemistrybiology.proteinProtein BindingJournal of Investigative Dermatology
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Rats bred for low aerobic capacity become promptly fatigued and have slow metabolic recovery after stimulated, maximal muscle contractions.

2012

AIM. Muscular fatigue is a complex phenomenon affected by muscle fiber type and several metabolic and ionic changes within myocytes. Mitochondria are the main determinants of muscle oxidative capacity which is also one determinant of muscle fatigability. By measuring the concentrations of intracellular stores of high-energy phosphates it is possible to estimate the energy production efficiency and metabolic recovery of the muscle. Low intrinsic aerobic capacity is known to be associated with reduced mitochondrial function. Whether low intrinsic aerobic capacity also results in slower metabolic recovery of skeletal muscle is not known. Here we studied the influence of intrinsic aerobic capac…

Magnetic Resonance SpectroscopyAnatomy and PhysiologyPhosphocreatineEvolutionary Selectionlcsh:MedicineIsometric exerciseBreedingmetaboliset sairaudetBiochemistrychemistry.chemical_compound0302 clinical medicineTriceps surae muscleMyocyteta315lcsh:ScienceMusculoskeletal System0303 health sciencesMultidisciplinarycomplex diseaseMuscle BiochemistryAnatomyAnimal ModelsHydrogen-Ion Concentrationmedicine.anatomical_structureaerobinen kapasiteettiMuscle FatigueMuscleaerobinen suorituskykymedicine.symptomMuscle contractionMuscle ContractionResearch Articlemedicine.medical_specialtyEvolutionary ProcessessupistusominaisuudetBioenergeticsPhosphocreatinePhosphates03 medical and health sciencesModel OrganismsInternal medicinePhysical Conditioning AnimalmedicineGeneticsAnimalsskeletal muscleAdaptationBiologyAerobic capacity030304 developmental biologyEvolutionary BiologyMuscle fatiguelcsh:RSkeletal muscleElectric StimulationRatsraajalihasEndocrinologyMetabolismcontractile propertieschemistryRatlcsh:QEnergy MetabolismPhysiological ProcessesAnimal Genetics030217 neurology & neurosurgeryPLoS ONE
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Systemic blockade of ACVR2B ligands attenuates muscle wasting in ischemic heart failure without compromising cardiac function

2020

Signaling through activin receptors regulates skeletal muscle mass and activin receptor 2B (ACVR2B) ligands are also suggested to participate in myocardial infarction (MI) pathology in the heart. In this study, we determined the effect of systemic blockade of ACVR2B ligands on cardiac function in experimental MI, and defined its efficacy to revert muscle wasting in ischemic heart failure (HF). Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) to study its effect on post-MI cardiac remodeling and on later HF. Cardiac function was determined with echocardiography, and myocardium analyzed with histological and biochemical methods for hypertrophy and fibrosis. Pharmacological blo…

Male0301 basic medicineCardiac function curvemedicine.medical_specialtyActivin Receptors Type IIMyocardial IschemiaMyostatinBiochemistryMuscle hypertrophyMice03 medical and health sciences0302 clinical medicineInternal medicineGeneticsmedicineAnimalsMyocyteMyocardial infarctionMolecular BiologyVentricular Remodelingbiologybusiness.industrySkeletal muscleHeartmedicine.disease3. Good healthBlockadeMice Inbred C57BLDisease Models AnimalMuscular Atrophy030104 developmental biologymedicine.anatomical_structureCardiologybiology.proteinbusiness030217 neurology & neurosurgeryACVR2BSignal TransductionTranscription FactorsBiotechnologyThe FASEB Journal
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Active acetylcholine receptors prevent the atrophy of skeletal muscles and favor reinnervation

2020

Denervation of skeletal muscles induces severe muscle atrophy, which is preceded by cellular alterations such as increased plasma membrane permeability, reduced resting membrane potential and accelerated protein catabolism. The factors that induce these changes remain unknown. Conversely, functional recovery following denervation depends on successful reinnervation. Here, we show that activation of nicotinic acetylcholine receptors (nAChRs) by quantal release of acetylcholine (ACh) from motoneurons is sufficient to prevent changes induced by denervation. Using in vitro assays, ACh and non-hydrolysable ACh analogs repressed the expression of connexin43 and connexin45 hemichannels, which prom…

Male0301 basic medicineCell Membrane PermeabilityNeuromuscular transmissionSkeletal muscleGeneral Physics and AstronomylihaksetasetyylikoliiniReceptors NicotinicConnexinsMembrane PotentialsMice0302 clinical medicineGanglia SpinalMyocytevälittäjäaineetlcsh:ScienceCells CulturedDenervationMultidisciplinaryChemistryQMuscle atrophy3. Good healthCell biologyMuscular AtrophyNicotinic agonistmedicine.anatomical_structuremedicine.symptomAcetylcholinemedicine.drugReinnervationScienceMice TransgenicArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesmedicineAnimalsskeletal muscleMuscle SkeletalAcetylcholine receptorsoluviestintäsomatic systemGeneral ChemistryAcetylcholineMice Inbred C57BLhermosolut030104 developmental biologynervous systemConnexin 43lcsh:Qsense organsSomatic systemlihassurkastumasairaudet030217 neurology & neurosurgeryNature Communications
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Telmisartan cardioprotects from the ischaemic/hypoxic damage through a miR‐1‐dependent pathway

2019

The aim of this study was to investigate whether telmisartan protects the heart from the ischaemia/reperfusion damage through a local microRNA-1 modulation. Studies on the myocardial ischaemia/reperfusion injury in vivo and on the cardiomyocyte hypoxia/reoxygenation damage in vitro were done. In vivo, male Sprague-Dawley rats administered for 3 weeks with telmisartan 12 mg/kg/d by gastric gavage underwent ischaemia/reperfusion of the left descending coronary artery. In these rats, infarct size measurement, ELISA, immunohistochemistry (IHC) and reverse transcriptase real-time polymerase chain reaction showed that expressions of connexin 43, potassium voltage-gated channel subfamily Q member …

Male0301 basic medicineCell SurvivalMyocardial InfarctionIschemiaConnexinMyocardial Reperfusion InjuryPharmacologymiR‐1telmisartanCell Lineconnexin 43Rats Sprague-Dawleyhypoxic H9c2 cells03 medical and health sciences0302 clinical medicineIn vivomedicineAnimalsBcl-2Myocytes CardiacKCNQ1ChemistryBcl‐2Original ArticlesCell BiologyTransfectionHypoxia (medical)medicine.diseasemiR-1Cell HypoxiaIn vitroRatsMicroRNAsmyocardial ischaemia/reperfusion030104 developmental biologyProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisKCNQ1 Potassium ChannelMolecular Medicinehypoxic H9c2 cellOriginal Articlemedicine.symptomTelmisartanReperfusion injurymedicine.drugJournal of Cellular and Molecular Medicine
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The early response of αB-crystallin to a single bout of aerobic exercise in mouse skeletal muscles depends upon fiber oxidative features

2019

Besides its substantial role in eye lens, αB-crystallin (HSPB5) retains fundamental function in striated muscle during physiological or pathological modifications. In this study, we aimed to analyse the cellular and molecular factors driving the functional response of HSPB5 protein in different muscles from mice subjected to an acute bout of non-damaging endurance exercise or in C2C12 myocytes upon exposure to pro-oxidant environment, chosen as “in vivo” and “in vitro” models of a physiological stressing conditions, respectively.To this end, red (GR) and white gastrocnemius (GW), as sources of slow-oxidative and fast-glycolytic/oxidative fibers, as well as the soleus (SOL), mainly composed …

Male0301 basic medicineMuscle Fibers SkeletalClinical BiochemistrySkeletal muscleFluorescent Antibody TechniqueOxidative phosphorylationFilaminBiochemistryMice03 medical and health sciences0302 clinical medicineSettore BIO/10 - BiochimicaPhysical Conditioning AnimalmedicineAnimalsMyocytePhosphorylationlcsh:QH301-705.5Actinlcsh:R5-920Settore BIO/16 - Anatomia UmanaMyogenesisChemistryOrganic ChemistryαB-crystallin phosphorylationalpha-Crystallin B ChainSkeletal muscleImmunohistochemistryEndurance exerciseCell biologyOxidative Stress030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)Oxidative streDesminMyofibrillcsh:Medicine (General)Oxidation-ReductionBiomarkers030217 neurology & neurosurgeryResearch PaperSignal TransductionRedox Biology
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Investigating and re-evaluating the role of glycogen synthase kinase 3 beta kinase as a molecular target for cardioprotection by using novel pharmaco…

2019

Aims Glycogen synthase kinase 3 beta (GSK3β) link with the mitochondrial Permeability Transition Pore (mPTP) in cardioprotection is debated. We investigated the role of GSK3β in ischaemia (I)/reperfusion (R) injury using pharmacological tools. Methods and results Infarct size using the GSK3β inhibitor BIO (6-bromoindirubin-3'-oxime) and several novel analogues (MLS2776-MLS2779) was determined in anaesthetized rabbits and mice. In myocardial tissue GSK3β inhibition and the specificity of the compounds was tested. The mechanism of protection focused on autophagy-related proteins. GSK3β localization was determined in subsarcolemmal (SSM) and interfibrillar mitochondria (IFM) isolated from Lang…

Male0301 basic medicinePhysiologyMyocardial InfarctionAutophagy-Related ProteinsMyocardial Reperfusion Injury030204 cardiovascular system & hematologyMitochondrionPharmacologyMitochondrial Membrane Transport ProteinsMitochondria HeartStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineReperfusion therapyPhysiology (medical)AnimalsMyocytes CardiacProtein Kinase InhibitorsGSK3BMice Knockoutchemistry.chemical_classificationCardioprotectionReactive oxygen speciesGlycogen Synthase Kinase 3 betaMolecular StructureMitochondrial Permeability Transition PoreChemistryKinaseMPTPIsolated Heart PreparationMice Inbred C57BLDisease Models Animal030104 developmental biologyMitochondrial permeability transition poreFemaleRabbitsCardiology and Cardiovascular MedicineCyclophilin DSignal TransductionCardiovascular Research
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Stable Oxidative Cytosine Modifications Accumulate in Cardiac Mesenchymal Cells From Type2 Diabetes Patients

2018

Rationale: Human cardiac mesenchymal cells (CMSCs) are a therapeutically relevant primary cell population. Diabetes mellitus compromises CMSC function as consequence of metabolic alterations and incorporation of stable epigenetic changes. Objective: To investigate the role of α-ketoglutarate (αKG) in the epimetabolic control of DNA demethylation in CMSCs. Methods and Results: Quantitative global analysis, methylated and hydroxymethylated DNA sequencing, and gene-specific GC methylation detection revealed an accumulation of 5-methylcytosine, 5-hydroxymethylcytosine, and 5-formylcytosine in the genomic DNA of human CMSCs isolated from diabetic donors. Whole heart genomic DNA analysis reveale…

Male0301 basic medicinePhysiologyPopulationheartBiologyMixed Function OxygenasesCytosineMice03 medical and health sciencesProto-Oncogene ProteinsfibroblastsHuman Umbilical Vein Endothelial CellsAnimalsHumansMyocytes CardiacEpigeneticsEnzyme InhibitorseducationCells CulturedEpigenomicsDemethylationeducation.field_of_studyDNA methylationDNA methylation; epigenomics; fibroblasts; heart; hyperglycemia; metabolism; physiology; cardiology and cardiovascular medicineMesenchymal Stem CellsSettore MED/13 - ENDOCRINOLOGIABase excision repairMolecular biologyThymine DNA GlycosylaseMice Inbred C57BLHEK293 Cells030104 developmental biologyDNA demethylationDiabetes Mellitus Type 2epigenomicsDNA methylationKetoglutaric AcidshyperglycemiaThymine-DNA glycosylaseCardiology and Cardiovascular MedicineOxidation-ReductionmetabolismCirculation Research
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Myocardial maladaptation to pressure overload in CB2 receptor-deficient mice

2019

Abstract Background Adaptation to aortic valve stenosis leads to myocardial hypertrophy, which has been associated with inflammation, fibrosis and activation of the endocannabinoid system. Since the endocannabinoid system and the CB2 receptor provide cardioprotection and modulate immune response in experimental ischemia, we investigated the role of CB2 in a mouse model of cardiac pressure overload. Methods Transverse aortic constriction was performed in CB2 receptor-deficient (Cnr2−/−) mice and their wild-type littermates (Cnr2+/+). After echocardiography and Millar left heart catheter hemodynamic evaluation hearts were processed for histological, cellular and molecular analyses. Results Th…

Male0301 basic medicinemedicine.medical_specialtyGenotypeFluorescent Antibody TechniqueBlood PressureCardiomegalyInflammation030204 cardiovascular system & hematologyProinflammatory cytokineReceptor Cannabinoid CB2Mice03 medical and health sciences0302 clinical medicineImmune systemFibrosisInternal medicineVentricular DysfunctionmedicineAnimalsMyocytes CardiacMolecular BiologyMice KnockoutPressure overloadCardioprotectionVentricular RemodelingChemistryMyocardiumHemodynamicsmedicine.diseaseImmunohistochemistryEndocannabinoid systemDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyFemaleInflammation Mediatorsmedicine.symptomCardiology and Cardiovascular MedicineMyofibroblastBiomarkersEndocannabinoidsJournal of Molecular and Cellular Cardiology
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