Search results for "Muscle atrophy"

showing 10 items of 47 documents

Prolonged exposure to microgravity modifies limb endpoint kinematics during the swing phase of human walking

2002

Many neurophysiological and behavioural studies suggested that the lower limb endpoint might be a centrally represented variable within the gravity reference frame and effectively controlled during the locomotion. This investigation examines the effects of prolonged exposure to microgravity upon lower limb endpoint kinematics. Seven cosmonauts were tested before and the 2nd day after a 6 month orbital mission. The spatio-temporal patterns of the limb extremity (malleolus) were analysed during the swing phase of the walk using a motion analysis system. Paths and velocity profiles of endpoint displacements were computed and compared for both the pre- and post-flight walking sessions. The resu…

Legmedicine.medical_specialtyMotion analysisWeightlessnessStance phasebusiness.industryMovementGeneral NeuroscienceWalkingKinematicsAnatomyMotor ActivitySwingNeurophysiologyMalleolusMuscle atrophyBiomechanical PhenomenaPeripheralPhysical medicine and rehabilitationmedicine.anatomical_structuremedicineHumansmedicine.symptombusinessNeuroscience Letters
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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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Muscle follistatin gene delivery increases muscle protein synthesis independent of periodical physical inactivity and fasting

2020

Blocking of myostatin and activins effectively counteracts muscle atrophy. However, the potential interaction with physical inactivity and fasting in the regulation of muscle protein synthesis is poorly understood. We used blockade of myostatin and activins by recombinant adeno-associated virus (rAAV)-mediated follistatin (FS288) overexpression in mouse tibialis anterior muscle. To investigate the effects on muscle protein synthesis, muscles were collected 7 days after rAAV-injection in the nighttime or in the daytime representing high and low levels of activity and feeding, respectively, or after overnight fasting, refeeding, or ad libitum feeding. Muscle protein synthesis was increased by…

Male0301 basic medicineFollistatinMuscle Proteinsphysical activitylihaksetMyostatinBiochemistryMice0302 clinical medicineTibialis anterior musclemedia_common2. Zero hungerbiologyChemistryactivinsFastingDependovirusMuscle atrophyCircadian RhythmMuscular Atrophymyostatinmedicine.symptomfyysinen aktiivisuusBiotechnologymedicine.medical_specialtyfastingmedia_common.quotation_subjectMechanistic Target of Rapamycin Complex 1Gene delivery03 medical and health sciencesPhysical Conditioning AnimalInternal medicineGeneticsmedicineAnimalsMolecular BiologypaastoPI3K/AKT/mTOR pathwaysolufysiologiaSarcolemmaJNK Mitogen-Activated Protein Kinasesmechanistic target of rapamycin proteinAppetiteGenetic TherapyMice Inbred C57BL030104 developmental biologyEndocrinologybiology.protein1182 Biochemistry cell and molecular biology3111 BiomedicineproteiinitEnergy Metabolismlihassurkastumasairaudet030217 neurology & neurosurgeryFollistatin
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Inhibition of Xanthine Oxidase by Allopurinol Prevents Skeletal Muscle Atrophy: Role of p38 MAPKinase and E3 Ubiquitin Ligases

2012

International audience; Abstract Top Alterations in muscle play an important role in common diseases and conditions. Reactive oxygen species (ROS) are generated during hindlimb unloading due, at least in part, to the activation of xanthine oxidase (XO). The major aim of this study was to determine the mechanism by which XO activation causes unloading-induced muscle atrophy in ratsand its possible prevention by allopurinol, a well-known inhibitor of this enzyme. For this purpose we studied one of the main redox sensitive signalling cascades involved in skeletal muscle atrophy i.e. p38 MAPKinaseand the expression of two well known muscle specific E3 ubiquitin ligases involved in proteolysis, …

MaleAgingAnatomy and Physiology[SDV]Life Sciences [q-bio]lcsh:MedicineMuscle ProteinsGene ExpressionHindlimbSignal transductionmedicine.disease_causep38 Mitogen-Activated Protein KinasesTripartite Motif Proteinschemistry.chemical_compound0302 clinical medicineMolecular cell biologySignaling in Cellular Processeslcsh:ScienceMusculoskeletal System0303 health sciencesMultidisciplinarySignaling cascadesMuscle BiochemistryAnimal ModelsMuscle atrophy3. Good healthMuscular Atrophymedicine.anatomical_structureBiochemistryHindlimb SuspensionMuscleMedicinemedicine.symptomCellular Typesmedicine.drugResearch Articlemedicine.medical_specialtyXanthine OxidaseMAPK signaling cascadesAllopurinolUbiquitin-Protein LigasesAllopurinolBiology03 medical and health sciencesAtrophyModel OrganismsInternal medicinemedicineAnimalsRats WistarXanthine oxidaseMuscle SkeletalBiology030304 developmental biologySoleus muscleMuscle CellsSKP Cullin F-Box Protein LigasesSuperoxide Dismutaselcsh:RSkeletal musclemedicine.diseaseRatsEnzyme ActivationOxidative StressEndocrinologychemistryRatlcsh:QPhysiological Processes030217 neurology & neurosurgeryOxidative stress
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Clobetasol promotes neuromuscular plasticity in mice after motoneuronal loss via sonic hedgehog signaling, immunomodulation and metabolic rebalancing

2021

AbstractMotoneuronal loss is the main feature of amyotrophic lateral sclerosis, although pathogenesis is extremely complex involving both neural and muscle cells. In order to translationally engage the sonic hedgehog pathway, which is a promising target for neural regeneration, recent studies have reported on the neuroprotective effects of clobetasol, an FDA-approved glucocorticoid, able to activate this pathway via smoothened. Herein we sought to examine functional, cellular, and metabolic effects of clobetasol in a neurotoxic mouse model of spinal motoneuronal loss. We found that clobetasol reduces muscle denervation and motor impairments in part by restoring sonic hedgehog signaling and …

MaleCancer ResearchPhysiology129 StrainBiochemistryMiceDatabases GeneticMedicineMyocyteMotor NeuronsNeuronal PlasticitySkeletalSmoothened ReceptorHedgehog signaling pathwayMuscle atrophyMitochondriaAstrogliosisNeuroprotective AgentsMusclemedicine.symptomInflammation MediatorsSignal TransductionCholera ToxinMice 129 StrainhedgehogImmunologyMotor ActivityNeuroprotectionArticleDatabasesCellular and Molecular NeurosciencesmoothenedGeneticAnimalsHumansHedgehog ProteinsMuscle SkeletalHedgehogGlucocorticoidsMuscle DenervationQH573-671Animalbusiness.industryAmyotrophic Lateral SclerosisGlial biologyCell Biologymedicine.diseaseSaporinsSpineMitochondria MuscleDisease Models AnimalclobetasolinflammationCase-Control StudiesDisease ModelsDiseases of the nervous systemCytologySmoothenedbusinessEnergy MetabolismNeuroscienceOpen Field Test
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mRNA levels for α-subunit of prolyl 4-hydroxylase and fibrillar collagens in immobilized rat skeletal muscle

1999

There is evidence that immobilization causes a decrease in total collagen synthesis in skeletal muscle within a few days. In this study, early immobilization effects on the expression of prolyl 4-hydroxylase (PH) and the main fibrillar collagens at mRNA and protein levels were investigated in rat skeletal muscle. The right hindlimb was immobilized in full plantar flexion for 1, 3, and 7 days. Steady-state mRNAs for α- and β-subunits of PH and type I and III procollagen, PH activity, and collagen content were measured in gastrocnemius and plantaris muscles. Type I and III procollagen mRNAs were also measured in soleus and tibialis anterior muscles. The mRNA level for the PH α-subunit decreas…

MaleDNA ComplementaryProtein ConformationPhysiologyProcollagen-Proline DioxygenaseDown-RegulationBiologyRats Sprague-DawleyImmobilizationchemistry.chemical_compoundHydroxyprolineBiosynthesisDownregulation and upregulationPhysiology (medical)Gene expressionmedicineAnimalsRNA MessengerMuscle Skeletalchemistry.chemical_classificationMessenger RNABase SequenceBody WeightSkeletal muscleOrgan SizeMuscle atrophyRatsMuscular Atrophymedicine.anatomical_structureBiochemistrychemistryCollagenmedicine.symptomGlycoproteinJournal of Applied Physiology
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Inhibition of autophagy rescues muscle atrophy in a LGMDD2 Drosophila model

2021

Limb-girdle muscular dystrophy D2 (LGMDD2) is an ultrarare autosomal dominant myopathy caused by mutation of the normal stop codon of the TNPO3 nuclear importin. The mutant protein carries a 15 amino acid C-terminal extension associated with pathogenicity. Here we report the first animal model of the disease by expressing the human mutant TNPO3 gene in Drosophila musculature or motor neurons and concomitantly silencing the endogenous expression of the fly protein ortholog. A similar genotype expressing wildtype TNPO3 served as a control. Phenotypes characterization revealed that mutant TNPO3 expression targeted at muscles or motor neurons caused LGMDD2-like phenotypes such as muscle degener…

MaleMutantBiochemistryAnimals Genetically ModifiedMutant proteinAutophagyGeneticsmedicineAnimalsHumansGene silencingMuscular dystrophyMyopathyMolecular BiologyMotor NeuronsbiologyMusclesAutophagyChloroquinebeta Karyopherinsmedicine.diseasebiology.organism_classificationMuscle atrophyCell biologySurvival RateDisease Models AnimalMuscular AtrophyDrosophila melanogasterPhenotypeMuscular Dystrophies Limb-GirdleInsect HormonesFemalemedicine.symptomDrosophila melanogasterLocomotionBiotechnologyThe FASEB Journal
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Expanding the clinical spectrum of hereditary fibrosing poikiloderma with tendon contractures, myopathy and pulmonary fibrosis due to FAM111B mutatio…

2015

Background Hereditary Fibrosing Poikiloderma (HFP) with tendon contractures, myopathy and pulmonary fibrosis (POIKTMP [MIM 615704]) is a very recently described entity of syndromic inherited poikiloderma. Previously by using whole exome sequencing in five families, we identified the causative gene, FAM111B (NM_198947.3), the function of which is still unknown. Our objective in this study was to better define the specific features of POIKTMP through a larger series of patients. Methods Clinical and molecular data of two families and eight independent sporadic cases, including six new cases, were collected. Results Key features consist of: (i) early-onset poikiloderma, hypotrichosis and hypoh…

MalePathologyMyopathyPulmonary FibrosisMedicine/Public HealthCell Cycle ProteinsGrowthHypotrichosisContracturesTendons030207 dermatology & venereal diseases0302 clinical medicineFibrosisPulmonary fibrosisSerineGenetics(clinical)Pharmacology (medical)TrypsinExomeChildGenetics (clinical)FAM111BSkinMedicine(all)0303 health sciencesMicroscopyMuscle WeaknessMusclesSkin Diseases GeneticGeneral MedicineMiddle AgedMagnetic Resonance ImagingMuscle atrophy3. Good healthMuscular AtrophyTissuesLiverChild PreschoolFemalemedicine.symptomAdultmedicine.medical_specialtyContractureAdolescentMolecular Sequence DataPoikiloderma03 medical and health sciencesPoikilodermaMuscular DiseasesmedicineHumansAdiposisAmino Acid SequenceCysteineExocrine pancreatic insufficiencyMyopathyMuscle Skeletal030304 developmental biologyMuscle contractureHypohidrosisSclerosisbusiness.industryResearchInfantProteinsmedicine.diseaseFibrosisGenesMutationSkin AbnormalitiesHypotrichosisExocrine Pancreatic Insufficiencybusiness
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Changes of sonographic, magnetic resonance tomographic, electromyographic, and histopathologic findings within a 2-month period of examinations after…

1998

This study compares sonographical, histopathological, magnetic resonance imaging (MRI), and electromyographical (EMG) findings following acute muscle denervation. We performed an experimental denervation of the supraspinatus and infraspinatus muscles on 35 New Zealand white rabbits by segment resection of the suprascapular nerve. The sonographical appearance of the supraspinatus muscle was followed and documented at short time intervals within a 2-month follow-up period. The sonographical, histopathological, and MRI changes due to denervation suggest a regular pattern. Apart from the reduction of the muscle diameter, there were considerable sonographical signs of denervation with an increas…

MalePathologymedicine.medical_specialtySupraspinatus muscleElectromyographySensitivity and Specificity030218 nuclear medicine & medical imaging03 medical and health sciences0302 clinical medicinemedicineAnimalsOrthopedics and Sports MedicinePeripheral NervesUltrasonographyDenervationMuscle Denervationmedicine.diagnostic_testElectromyographybusiness.industryMagnetic resonance imagingGeneral MedicineAnatomySuprascapular nerveMagnetic Resonance ImagingMuscle DenervationMuscle atrophy3. Good healthMuscular Atrophymedicine.anatomical_structureSurgeryRabbitsmedicine.symptombusiness030217 neurology & neurosurgeryFollow-Up StudiesReinnervationArchives of Orthopaedic and Trauma Surgery
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Altered REDD1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy

2011

Type 1 diabetes, if poorly controlled, leads to skeletal muscle atrophy, decreasing the quality of life. We aimed to search highly responsive genes in diabetic muscle atrophy in a common diabetes model and to further characterize associated signaling pathways. Mice were killed 1, 3, or 5 wk after streptozotocin or control. Gene expression of calf muscles was analyzed using microarray and protein signaling with Western blotting. We identified translational repressor protein REDD1 (regulated in development and DNA damage responses) that increased seven- to eightfold and was associated with muscle atrophy in diabetes. The diabetes-induced increase in REDD1 was confirmed at the protein level. …

Malemedicine.medical_specialtyMAP Kinase Signaling SystemPhysiologyEndocrinology Diabetes and MetabolismFOXO1P70-S6 Kinase 1MyostatinBiologyMiceRandom Allocation03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicinemedicineAnimalsRNA MessengerPhosphorylationMuscle SkeletalProtein kinase BPI3K/AKT/mTOR pathwayOligonucleotide Array Sequence Analysis030304 developmental biology0303 health sciencesForkhead Box Protein O1Gene Expression ProfilingTOR Serine-Threonine KinasesUbiquitinationForkhead Transcription FactorsOrgan SizeMyostatinProtein ubiquitinationMuscle atrophyMuscular AtrophyDNA Repair EnzymesDiabetes Mellitus Type 1EndocrinologyGene Expression Regulationbiology.proteinPhosphorylationmedicine.symptomProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryTranscription FactorsAmerican Journal of Physiology-Endocrinology and Metabolism
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