Search results for "Myogenesis"

showing 10 items of 42 documents

The metalloproteinase-disintegrin ADAM10 is exclusively expressed by type I muscle fibers.

2008

ADAM10 (Kuzbanian) is a member of a recently discovered family of membrane-anchored metalloproteinases with a complex and conserved domain structure. In part, these metalloproteinases have been implicated in muscle formation. Herein the expression pattern of ADAM10 in human skeletal muscle was studied. ADAM10 was found to be present in human myoblasts and to be exclusively expressed in type I fibers, suggesting that it may be critical in muscle fiber differentiation.

PhysiologyADAM10Matrix metalloproteinaseCellular and Molecular NeuroscienceADAM10 ProteinPhysiology (medical)DisintegrinmedicineMyocyteHumansAdenosine TriphosphatasesMetalloproteinasebiologyMyosin Heavy ChainsMyogenesisChemistrySkeletal muscleMembrane ProteinsCell biologyADAM Proteinsmedicine.anatomical_structureMuscle Fibers Slow-TwitchBiochemistrybiology.proteinNeurology (clinical)Amyloid Precursor Protein SecretasesITGA7Musclenerve
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MICROWAVE EFFECTS ON ACETYLCHOLINE-INDUCED CHANNELS IN CULTURED CHICK MYOTUBES

1988

The behavior of cultured myotubes from chick embryos exposed to microwaves has been experimentally analyzed. Recordings of acetylcholine-induced currents have been obtained via patch-clamp techniques using both cell-attached (single-channel current recording) and whole-cell (total current recording) configurations. During the exposure to low-power microwaves the frequency of the ACh-activated single channel openings decreased, while the ACh-induced total current showed a faster falling phase. Channel open time and conductance were not affected by microwave irradiation. It is concluded that the exposure to microwaves increases the rate of desensitization and decreases the channel opening pro…

PhysiologyMyogenesisChemistryMusclesBiophysicsPhase (waves)ConductanceChick EmbryoGeneral MedicineAnatomyIn Vitro TechniquesElectromagnetic radiationAcetylcholineIon ChannelsDesensitization (telecommunications)medicineBiophysicsAnimalsRadiology Nuclear Medicine and imagingacetylcholine receptor; microwave irradiationCurrent (fluid)MicrowavesMicrowaveAcetylcholinemedicine.drug
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Bortezomib Partially Improves Laminin α2 Chain–Deficient Muscular Dystrophy

2014

Congenital muscular dystrophy, caused by mutations in LAMA2 (the gene encoding laminin α2 chain), is a severe and incapacitating disease for which no therapy is yet available. We have recently demonstrated that proteasome activity is increased in laminin α2 chain-deficient muscle and that treatment with the nonpharmaceutical proteasome inhibitor MG-132 reduces muscle pathology in laminin α2 chain-deficient dy(3K)/dy(3K) mice. Here, we explore the use of the selective and therapeutic proteasome inhibitor bortezomib (currently used for treatment of relapsed multiple myeloma and mantle cell lymphoma) in dy(3K)/dy(3K) mice and in congenital muscular dystrophy type 1A muscle cells. Outcome measu…

Proteasome Endopeptidase ComplexApoptosisBiologyPathology and Forensic MedicineBortezomibmedicineAnimalsMyocyteMuscular dystrophyCells CulturedMultiple myelomaMuscle CellsMyogenesisBortezomibMusclesBody WeightMuscular Dystrophy Animalmedicine.diseaseBoronic AcidsFibrosisSurvival AnalysisMice Inbred C57BLDisease Models AnimalMicroRNAsGene Expression RegulationOrgan SpecificityPyrazinesCongenital muscular dystrophyCancer researchProteasome inhibitorMantle cell lymphomaLamininLocomotionmedicine.drugThe American Journal of Pathology
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Erbb2 regulates neuromuscular synapse formation and is essential for muscle spindle development

2003

Neuregulins and their Erbb receptors have been implicated in neuromuscular synapse formation by regulating gene expression in subsynaptic nuclei. To analyze the function of Erbb2 in this process, we have inactivated the Erbb2 gene in developing muscle fibers by Cre/Lox-mediated gene ablation. Neuromuscular synapses form in the mutant mice, but the synapses are less efficient and contain reduced levels of acetylcholine receptors. Surprisingly, the mutant mice also show proprioceptive defects caused by abnormal muscle spindle development. Sensory Ia afferent neurons establish initial contact with Erbb2-deficient myotubes. However, functional spindles never develop. Taken together, our data su…

Receptor ErbB-2Muscle spindleNeuromuscular JunctionMice TransgenicBiologySynaptic TransmissionNeuromuscular junctionSynapseMiceErbB ReceptorsmedicineAnimalsHumansMuscle SkeletalPromoter Regions Geneticskin and connective tissue diseasesMuscle SpindlesMolecular BiologyAcetylcholine receptorMice KnockoutAfferent PathwaysMyogenesisGenes erbB-2ActinsMice Mutant StrainsCell biologyMice Inbred C57BLmedicine.anatomical_structureSilent synapseNeuregulinSignal TransductionDevelopmental BiologyDevelopment
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Resveratrol initiates differentiation of mouse skeletal muscle-derived C2C12 myoblasts.

2012

Resveratrol is one of the most widely studied bio-active plant polyphenols. While its effect on endothelial blood vessel cells, cancer cells, inflammatory processes and neurodegenerative events is well documented, little is known about the implication of this phytophenol in differentiating processes, particularly in skeletal muscle cells. Here, we report the effects of resveratrol on mouse skeletal muscle-derived cells (C2C12) in either a nondifferentiated (myoblasts) or differentiated state (myotubes) by evaluating resveratrol uptake, cell proliferation, changes in cell shape, and the expression of genes encoding muscle-specific transcription factors or contractile proteins. Resveratrol: (…

Transcription GeneticCellular differentiationMyoblasts SkeletalMuscle Fibers SkeletalBiologyResveratrolMyosinsBiochemistryCell Linechemistry.chemical_compoundMiceStilbenesmedicineMyocyteAnimalsCell ShapeMyogeninCell ProliferationPharmacologyMyogenesisfood and beveragesSkeletal muscleCell DifferentiationMolecular biologyMicroRNAsmedicine.anatomical_structurechemistryResveratrolCancer cellC2C12Transcription FactorsBiochemical pharmacology
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Alix protein is substrate of Ozz-E3 ligase and modulates actin remodeling in skeletal muscle

2012

Alix/AIP1 is a multifunctional adaptor protein that participates in basic cellular processes, including membrane trafficking and actin cytoskeleton assembly, by binding selectively to a variety of partner proteins. However, the mechanisms regulating Alix turnover, subcellular distribution, and function in muscle cells are unknown. We now report that Alix is expressed in skeletal muscle throughout myogenic differentiation. In myotubes, a specific pool of Alix colocalizes with Ozz, the substrate-binding component of the muscle-specific ubiquitin ligase complex Ozz-E3. We found that interaction of the two endogenous proteins in the differentiated muscle fibers changes Alix conformation and pro…

Ubiquitin-Protein LigasesMuscle Fibers Skeletalmacromolecular substancesBiochemistryCell LineMiceCell MovementTwo-Hybrid System TechniquesmedicineCell AdhesionAnimalsProtein Interaction Domains and MotifsPseudopodiaMuscle SkeletalMolecular BiologyActinMice KnockoutbiologyMyogenesisSettore BIO/16 - Anatomia UmanaCalcium-Binding ProteinsUbiquitinationActin remodelingSkeletal muscleUbiquitin-Protein Ligase ComplexesCell BiologyActin cytoskeletonUbiquitin ligaseCell biologyRepressor ProteinsActin CytoskeletonProtein Transportmedicine.anatomical_structureUbiquitin ligase complexbiology.proteinCell Migration Myogenesis Skeletal Muscle Ubiquitin Ligase Ubiquitination Alix F-actin Ozz-E3 Ubiquitin Ligase Skeletal Muscle CellsCortactinCortactinProtein Binding
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Preclinical characterization of antagomiR-218 as a potential treatment for myotonic dystrophy

2021

Myotonic dystrophy type 1 (DM1) is a rare neuromuscular disease caused by expansion of unstable CTG repeats in a non-coding region of the DMPK gene. CUG expansions in mutant DMPK transcripts sequester MBNL1 proteins in ribonuclear foci. Depletion of this protein is a primary contributor to disease symptoms such as muscle weakness and atrophy and myotonia, yet upregulation of endogenous MBNL1 levels may compensate for this sequestration. Having previously demonstrated that antisense oligonucleotides against miR-218 boost MBNL1 expression and rescue phenotypes in disease models, here we provide preclinical characterization of an antagomiR-218 molecule using the HSALR mouse model and patient-d…

antisense oligonucleotidetissue distributionRM1-950BiologyMyotonic dystrophyTranscriptomechemistry.chemical_compoundalternative splicingtranscriptomicsAtrophyDrug DiscoverymicroRNAmedicineMBNL1AntagomirCTG repeat expansionstherapeutic gene modulationCTG repeat expansions MBNL1 protein alternative splicing antisense oligonucleotide microRNAs myotonic dystrophy therapeutic gene modulation tissue distribution transcriptomicsmyotonic dystrophyMyogenesisMyotoniamedicine.diseasemicroRNAschemistryCancer researchMolecular MedicineOriginal ArticleTherapeutics. PharmacologyMBNL1 protein
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Musashi-2 contributes to myotonic dystrophy muscle dysfunction by promoting excessive autophagy through miR-7 biogenesis repression

2021

Skeletal muscle symptoms strongly contribute to mortality of myotonic dystrophy type 1 (DM1) patients. DM1 is a neuromuscular genetic disease caused by CTG repeat expansions that, upon transcription, sequester the Muscleblind-like family of proteins and dysregulate alternative splicing of hundreds of genes. However, mis-splicing does not satisfactorily explain muscle atrophy and wasting, and several other contributing factors have been suggested, including hyperactivated autophagy leading to excessive catabolism. MicroRNA ( miR ) -7 has been demonstrated to be necessary and sufficient to repress the autophagy pathway in cell models of the disease, but the origin of its low levels in DM1 was…

autophagyMSI2 antisense oligonucleotides autophagy miR-7 muscle atrophy muscle dysfunction myotonic dystrophy myotubesRM1-950BiologyMyotonic dystrophyMSI2chemistry.chemical_compoundDrug DiscoverymedicineMyocyteGene silencingMBNL1muscle dysfunctionmyotonic dystrophyMyogenesisAutophagymiR-7Skeletal musclemedicine.diseaseMuscle atrophyCell biologymedicine.anatomical_structurechemistryMolecular MedicineTherapeutics. Pharmacologyantisense oligonucleotidesmedicine.symptomMolecular Therapy - Nucleic Acids
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Exercise-Induced Activation and Translocation of αB-Crystallin in Skeletal Muscle Depends upon Fiber Type and Oxidative Stress

2016

Alpha B-crystallin (CRYAB) is a member of the small heat shock proteins implicated in various biological functions, particularly in skeletal muscle tissue [1], where it results to be modulated following exercise-induced reactive oxygen species (ROS) [2]. In this work we aimed to analyse the CRYAB response to acute exercise with respect muscle fiber composition and to identify the underlying molecular mechanism by the utilization of the C2C12 “in vitro” cellular model. Our results highlighted as acute exercise determines a specific increase of phospho-CRYAB both in the red, but not white, gastrocnemius (GS), with an higher amount of oxidative and oxidative-glycolytic fibers, and in soleus (S…

chemistry.chemical_classificationReactive oxygen speciesMyogenesisSkeletal muscleOxidative phosphorylationBiologymedicine.disease_causeBiochemistryCell biologymedicine.anatomical_structureBiochemistrychemistryPhysiology (medical)medicineROCK1ROCK2CytoskeletonOxidative stressFree Radical Biology and Medicine
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Effects of combined hormone replacement therapy or its effective agents on the IGF-1 pathway in skeletal muscle.

2010

Objectives To investigate the effects of combined hormone replacement therapy (HRT) and its effective agents on the IGF-1 signaling pathway. Design and methods To examine the effects of HRT on skeletal muscle in vivo, we utilized pre- and post-intervention samples from a randomized double blinded trial with 50–57-year-old women. The intervention included the year-long use of either HRT preparation (2 mg 17β-estradiol, E2; 1 mg norethisterone acetate, NETA, n = 10) or placebo (CO, n = 9). Microarray technology and quantitative PCR (qPCR) were used to study the expression of insulin-like growth factor I (IGF-1) and its splice variants as well as IGF-1 receptor, Akt1, mTOR, FOXO1, FOXO3, atrog…

estradioliTranscription GeneticEndocrinology Diabetes and MetabolismMuscle Fibers SkeletalEstrogen receptorpostmenopausal womenMuscle ProteinsFOXO1Receptor IGF Type 10302 clinical medicineEndocrinologyProtein IsoformsTestosteroneInsulin-Like Growth Factor IReceptorRandomized Controlled Trials as Topic0303 health sciencesEstradiolMyogenesisForkhead Box Protein O1TOR Serine-Threonine KinasesEstrogen Replacement TherapyForkhead Box Protein O3Forkhead Transcription FactorsMiddle Agedmedicine.anatomical_structureReceptors EstrogenReceptors AndrogenFemalemedicine.medical_specialtynorethisterone acetate030209 endocrinology & metabolismBiologypostmenopausaalinen nainen03 medical and health sciencesInternal medicinemedicineHumansnoretisteroniasetaattiluurankolihasskeletal muscleMuscle SkeletalProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologyhormonikorvaushoitoSKP Cullin F-Box Protein LigasesSkeletal muscleAndrogen receptorNorethindrone AcetateEndocrinologyHormone replacement therapyIGF-1 signalointiNorethindroneIGF-1 signalingProto-Oncogene Proteins c-aktGrowth hormoneIGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society
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