Search results for "MICE"

showing 10 items of 6027 documents

SOX2 expression diminishes with ageing in several tissues in mice and humans.

2017

SOX2 (Sex-determining region Y box 2) is a transcription factor expressed in several foetal and adult tissues and its deregulated activity has been linked to chronic diseases associated with ageing. Nevertheless, the level of SOX2 expression in aged individuals at the tissue level has not previously been examined. In this work, we show that SOX2 expression decreases significantly in the brain with ageing, in both humans and rodents. The administration of resveratrol for 6 months in mice partly attenuated this reduction. We also identified an age-related decline in SOX2 mRNA and protein expression in several other organs, namely, the lung, heart, kidney, spleen and liver. Moreover, periphera…

0301 basic medicineAdultMalemedicine.medical_specialtyAgingSOX2SpleenResveratrolBiologyPeripheral blood mononuclear cellGene Expression Regulation Enzymologic03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineSOX2stomatognathic systemInternal medicinemedicineAnimalsHumansCyclin-Dependent Kinase Inhibitor p16Aged 80 and overKidneyMessenger RNASOXB1 Transcription FactorsfungiMiddle AgedAgeing030104 developmental biologymedicine.anatomical_structureEndocrinologychemistryAgeingOrgan Specificityembryonic structuresLeukocytes MononuclearBiomarker (medicine)Femalesense organsbiological phenomena cell phenomena and immunity030217 neurology & neurosurgeryBiomarkersDevelopmental BiologyMechanisms of ageing and development
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Neuropeptide Y (NPY) in cerebrospinal fluid from patients with Huntington's Disease: increased NPY levels and differential degradation of the NPY1-30…

2016

Huntington's disease (HD) is an inherited and fatal polyglutamine neurodegenerative disorder caused by an expansion of the CAG triplet repeat coding region within the HD gene. Progressive dysfunction and loss of striatal GABAergic medium spiny neurons (MSNs) may account for some of the characteristic symptoms in HD patients. Interestingly, in HD, MSNs expressing neuropeptide Y (NPY) are spared and their numbers is even up-regulated in HD patients. Consistent with this, we report here on increased immuno-linked NPY (IL-NPY) levels in human cerebrospinal fluid (hCSF) from HD patients (Control n = 10; early HD n = 9; mid HD n = 11). As this antibody-based detection of NPY may provide false pos…

0301 basic medicineAdultMalemedicine.medical_specialtyCathepsin DDynorphinMedium spiny neuronBiochemistry03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineCerebrospinal fluidHuntington's diseaseInternal medicinemental disordersmedicineAnimalsHumansNeuropeptide YNeprilysinAgedThimet oligopeptidaseChemistryMiddle Agedmedicine.diseaseNeuropeptide Y receptorPeptide FragmentsRats030104 developmental biologyEndocrinologyHEK293 CellsHuntington DiseaseProteolysisFemale030217 neurology & neurosurgeryBiomarkersJournal of neurochemistry
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IGF-1 Haploinsufficiency Causes Age-Related Chronic Cochlear Inflammation and Increases Noise-Induced Hearing Loss

2021

This article belongs to the Collection Insulin-Like Growth Factors in Development, Cancers and Aging.

0301 basic medicineAgingApoptosisHaploinsufficiencyMice0302 clinical medicineBiology (General)Insulin-Like Growth Factor ICell DeathapoptosisGeneral Medicine3. Good healthCochleaCytokinesmedicine.symptomHaploinsufficiencyNoise-induced hearing lossmedicine.medical_specialtyHeterozygoteHearing lossQH301-705.5InflammationArticleARHLProinflammatory cytokine03 medical and health sciencesInternal medicinemedicineotorhinolaryngologic diseasesAnimalsRNA MessengerProtein kinase BCochleaInflammationbusiness.industryGene Expression ProfilingAKTTGFβ1Auditory Thresholdmedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologyGene Expression RegulationHearing Loss Noise-InducedAgeingSynapsesIL1βJNKbusinessNoise030217 neurology & neurosurgeryBiomarkersNIHL
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Electrical activity controls area-specific expression of neuronal apoptosis in the mouse developing cerebral cortex

2017

Programmed cell death widely but heterogeneously affects the developing brain, causing the loss of up to 50% of neurons in rodents. However, whether this heterogeneity originates from neuronal identity and/or network-dependent processes is unknown. Here, we report that the primary motor cortex (M1) and primary somatosensory cortex (S1), two adjacent but functionally distinct areas, display striking differences in density of apoptotic neurons during the early postnatal period. These differences in rate of apoptosis negatively correlate with region-dependent levels of activity. Disrupting this activity either pharmacologically or by electrical stimulation alters the spatial pattern of apoptos…

0301 basic medicineAgingMouseStimulationCell CountSomatosensory systemMice0302 clinical medicineAnesthesiaBiology (General)whisker deafferentationCerebral CortexNeuronsNeocortexCaspase 3General NeuroscienceQRapoptosisMotor CortexGeneral MedicineAnatomyactivity patternsmedicine.anatomical_structurecell deathCerebral cortexMedicinePrimary motor cortexMotor cortexResearch ArticleProgrammed cell deathQH301-705.5ScienceBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesmedicineAnimalsSensory deprivationdevelopmentGeneral Immunology and MicrobiologySomatosensory CortexElectrophysiological Phenomena030104 developmental biologyDevelopmental Biology and Stem Cellsnervous systemAnimals NewbornNeuroscience030217 neurology & neurosurgeryNeuroscienceeLife
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Adult rat myelin enhances axonal outgrowth from neural stem cells.

2018

Axon regeneration after spinal cord injury (SCI) is attenuated by growth inhibitory molecules associated with myelin. We report that rat myelin stimulated the growth of axons emerging from rat neural progenitor cells (NPCs) transplanted into sites of SCI in adult rat recipients. When plated on a myelin substrate, neurite outgrowth from rat NPCs and from human induced pluripotent stem cell (iPSC)-derived neural stem cells (NSCs) was enhanced threefold. In vivo, rat NPCs and human iPSC-derived NSCs extended greater numbers of axons through adult central nervous system white matter than through gray matter and preferentially associated with rat host myelin. Mechanistic investigations excluded …

0301 basic medicineAgingNeuronalNudeMessengerNeurodegenerativeInbred C57BLRegenerative MedicineMedical and Health SciencesMyelinMiceNeural Stem CellsStem Cell Research - Nonembryonic - HumanCyclic AMPAxonPhosphorylationGray MatterInduced pluripotent stem cellExtracellular Signal-Regulated MAP KinasesSpinal Cord InjuryMyelin SheathInbred F344Neuronal growth regulator 1Stem Cell Research - Induced Pluripotent Stem Cell - HumanChemistryGeneral MedicineBiological SciencesWhite MatterNeural stem cellCell biologymedicine.anatomical_structureSpinal Cord5.1 PharmaceuticalsNeurologicalFemaleStem Cell Research - Nonembryonic - Non-HumanDevelopment of treatments and therapeutic interventionsPhysical Injury - Accidents and Adverse EffectsNeuriteCell Adhesion Molecules NeuronalCentral nervous systemNeuronal OutgrowthArticleWhite matter03 medical and health sciencesRats NudemedicineAnimalsHumansRNA MessengerStem Cell Research - Embryonic - HumanTraumatic Head and Spine InjuryTransplantationStem Cell Research - Induced Pluripotent Stem CellNeurosciencesStem Cell ResearchRats Inbred F344AxonsRatsMice Inbred C57BL030104 developmental biologynervous systemChondroitin Sulfate ProteoglycansRNACell Adhesion Molecules
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Decreased bioavailability of nitric oxide in aorta from ovariectomized senescent mice. Role of cyclooxygenase.

2015

This study investigates the effects of aging and/or ovariectomy on vascular reactivity to thromboxane A2 (TXA2) receptor stimulation with U46619, and the modulation by nitric oxide (NO) and cyclooxygenase (COX) in aorta from female senescence-accelerated mice (SAMP8) and from senescence resistant mice (SAMR1). Five-month-old female SAMR1 and SAMP8 were divided into three groups: sham-operated, ovariectomized and ovariectomized plus estradiol. Twenty-eight days after surgery, thoracic aortic rings were mounted for isometric recording of tension and concentration-response curves for U46619 (10(-10)-3 × 10(-7) M) were performed in the absence and in the presence of the NO synthase inhibitor N(…

0301 basic medicineAgingReceptors ThromboxaneAorta Thoracic030204 cardiovascular system & hematologyBiochemistrychemistry.chemical_compoundThromboxane A2Mice0302 clinical medicineEndocrinologySuperoxidesThoracic aortaVasoconstrictor AgentsbiologyEstradiolSuperoxideEstrogen Replacement TherapyAge FactorsOvariectomized ratFemaleMenopauseSignal Transductionmedicine.medical_specialtymedicine.drug_classOvariectomyDown-RegulationNitric OxideNitric oxide03 medical and health sciencesThromboxane A2medicine.arteryInternal medicineGeneticsmedicineAnimalsCyclooxygenase InhibitorsMolecular BiologyAortaDose-Response Relationship Drugbusiness.industryCell BiologyEnzyme ActivationOxidative Stress030104 developmental biologyEndocrinologychemistryEstrogenProstaglandin-Endoperoxide SynthasesVasoconstrictionbiology.proteinCyclooxygenaseNitric Oxide SynthasebusinessExperimental gerontology
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Intensified mitophagy in skeletal muscle with aging is downregulated by PGC-1alpha overexpression in vivo.

2018

Mitochondrial dysfunction plays an important role in the etiology of age-related muscle atrophy known as sarcopenia. PGC-1α is positioned at the center of crosstalk in regulating mitochondrial quality control, but its role in mitophagy in aged skeletal muscle is currently unclear. The present study investigated the effects of aging and PGC-1α overexpression via in vivo DNA transfection on key mitophagy protein markers, as well as mitochondrial dynamics related proteins, metabolic function and antioxidant capacity in mouse muscle. C57BL/6J mice at the age of 2 mo (young, Y; N = 14) and 24 mo (old, O; N = 14) were transfected in vivo with either PGC-1α DNA (OE, N = 7) or GFP (N = 7) into the …

0301 basic medicineAgingUbiquitin-Protein LigasesPINK1MitochondrionBiochemistryMitochondrial DynamicsGTP Phosphohydrolases03 medical and health sciencesMice0302 clinical medicineIn vivoPhysiology (medical)MitophagymedicineAnimalsMuscle SkeletalChemistryMitophagySkeletal muscleTransfectionmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMuscle atrophyCell biologyMitochondriaOxidative Stress030104 developmental biologymedicine.anatomical_structureGene Expression RegulationSarcopeniaBeclin-1medicine.symptomProtein Kinases030217 neurology & neurosurgeryFree radical biologymedicine
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Biological and biophysics aspects of metformin-induced effects: cortex mitochondrial dysfunction and promotion of toxic amyloid pre-fibrillar aggrega…

2016

The onset of Alzheimer disease (AD) is influenced by several risk factors comprising diabetes. Within this context, antidiabetic drugs, including metformin, are investigated for their effect on AD. We report that in the C57B6/J mice, metformin is delivered to the brain where activates AMP-activated kinase (AMPK), its molecular target. This drug affects the levels of β- secretase (BACE1) and β-amyloid precursor protein (APP), promoting processing and aggregation of β-amyloid (Aβ), mainly in the cortex region. Moreover, metformin induces mitochondrial dysfunction and cell death by affecting the level and conformation of Translocase of the Outer Membrane 40 (TOM40), voltage-dependent anion-sel…

0301 basic medicineAgingmedicine.medical_specialtyMitochondrial poreAmyloidTranslocase of the outer membraneContext (language use)AMP-Activated Protein KinasesBiologyAmyloid beta-Protein PrecursorMice03 medical and health sciences0302 clinical medicineβ-amyloid aggregationAlzheimer DiseaseHexokinaseInternal medicine?-amyloid aggregationmitochondrial dysfunctionmedicineAnimalsHypoglycemic Agentsmitochondrial poresMitochondrial transportAmyloid beta-PeptidesVoltage-Dependent Anion Channel 1BrainAMPKcell degenerationCell BiologyAlzheimer's diseasemedicine.diseaseMitochondriaMetformin030104 developmental biologyEndocrinologyAmyloid Precursor Protein SecretasesAlzheimer's diseasemetforminVDAC1030217 neurology & neurosurgeryResearch Papermedicine.drug
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Overexpression of glucose 6 phosphate dehydrogenase preserves mouse pancreatic beta cells function until late in life.

2021

NAD(P)H donates electrons for reductive biosynthesis and antioxidant defense across all forms of life. Glucose-6- phosphate dehydrogenase (G6PD) is a critical enzyme to provide NADPH. G6PD deficiency is present in more than 400 million people worldwide. This enzymopathy provides protection against malaria but sensitizes cells to oxidative stressors. Oxidative stress has been involved in the pathogenesis of the diabetic complications and several studies have provided evidences of a link between G6PD deficiency and type 2 diabetes (T2D). We hypothesized that a moderate overexpression of G6PD (G6PD-Tg) could protect β-cells from age-associated oxidative stress thus reducing the risk of develop…

0301 basic medicineAgingmedicine.medical_specialtyOxidative phosphorylationType 2 diabetesGlucosephosphate Dehydrogenasemedicine.disease_causeBiochemistry03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinehemic and lymphatic diseasesPhysiology (medical)Internal medicineDiabetes mellitusInsulin-Secreting Cellsparasitic diseasesNADPHmedicineGlucose-6-phosphate dehydrogenaseAnimalsPancreatic isletsDiabetesWild typenutritional and metabolic diseasesmedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologymedicine.anatomical_structureGlucosephosphate Dehydrogenase DeficiencychemistryDiabetes Mellitus Type 2Oxidative stressPancreas030217 neurology & neurosurgeryOxidative stressFree radical biologymedicine
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A novel microglial subset plays a key role in myelinogenesis in developing brain.

2017

Microglia are resident macrophages of the central nervous system that contribute to homeostasis and neuroinflammation. Although known to play an important role in brain development, their exact function has not been fully described. Here, we show that in contrast to healthy adult and inflammation-activated cells, neonatal microglia show a unique myelinogenic and neurogenic phenotype. A CD11c(+) microglial subset that predominates in primary myelinating areas of the developing brain expresses genes for neuronal and glial survival, migration, and differentiation. These cells are the major source of insulin-like growth factor 1, and its selective depletion from CD11c(+) microglia leads to impa…

0301 basic medicineAgingmedicine.medical_treatmentNews & ViewsInsulin-Like Growth Factor IMyelin SheathCell AggregationNeural PlateMicrogliaACTIVATED MICROGLIAGeneral NeuroscienceExperimental autoimmune encephalomyelitisNeurogenesisIGF1BrainGene Expression Regulation DevelopmentalADULT BRAINUp-RegulationALZHEIMERS-DISEASEmedicine.anatomical_structureEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISMyelinogenesisGROWTHFemaleMicrogliaCNSEncephalomyelitis Autoimmune ExperimentalNeurogenesisCentral nervous systemCD11cBiologyGeneral Biochemistry Genetics and Molecular BiologyDEPENDENT MANNER03 medical and health sciencesmedicinePOSTNATAL-DEVELOPMENTAnimalsMolecular BiologyNeuroinflammationGeneral Immunology and MicrobiologyCD11cGrowth factorGene Expression ProfilingCENTRAL-NERVOUS-SYSTEMmedicine.diseaseGALECTIN-1CD11c AntigenMice Inbred C57BL030104 developmental biologynervous systemAnimals NewbornImmunologymyelinogenesisNeuroscienceBiomarkersThe EMBO journal
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