Search results for "TRANSGENIC MICE"

showing 10 items of 17 documents

Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice

2017

Amyloid-β (Aβ) deposition is one of the hallmarks of the amyloid hypothesis in Alzheimer’s disease (AD). Mouse models using APP-transgene overexpression to generate amyloid plaques have shown to model only certain parts of the disease. The extent to which the data from mice can be transferred to man remains controversial. Several studies have shown convincing treatment results in reducing Aβ and enhancing cognition in mice but failed totally in human. One model-dependent factor has so far been almost completely neglected: the endogenous expression of mouse APP and its effects on the transgenic models and the readout for therapeutic approaches. Here, we report that hAPP-transgenic models of …

0301 basic medicineGenetically modified mouseMaleMurine amyloid-betaBACE1-ASMice TransgenicPlaque Amyloidlcsh:RC346-429Pathology and Forensic Medicine03 medical and health sciencesCellular and Molecular NeuroscienceAmyloid beta-Protein Precursor0302 clinical medicineMeningesAmyloid precursor proteinMedicineAnimalsHumansTransgenic miceSenile plaqueslcsh:Neurology. Diseases of the nervous systemNeuronsAmyloid beta-Peptidesbiologybusiness.industryAmyloidosisResearchP3 peptideBrainAmyloidosismedicine.diseasePeptide FragmentsBiochemistry of Alzheimer's diseaseAstrogliosisCell biologyMice Inbred C57BL030104 developmental biologyCaspasesAmyloid precursor proteinMutationbiology.proteinAbetaFemaleNeurology (clinical)businessNeuroscienceAlzheimer’s disease030217 neurology & neurosurgery
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Srebf2 Locus Overexpression Reduces Body Weight, Total Cholesterol and Glucose Levels in Mice Fed with Two Different Diets

2020

Macronutrients represent risk factors for hyperlipidemia or diabetes. Lipid alterations and type 2 diabetes mellitus are global health problems. Overexpression of sterol regulatory element-binding factor (Srebf2) in transgenic animals is linked to elevated cholesterol levels and diabetes development. We investigated the impact of increased Srebf2 locus expression and the effects of control and high-fat, high-sucrose (HFHS) diets on body weight, glucose and lipid metabolisms in transgenic mice (S-mice). Wild type (WT) and S-mice were fed with both diets for 16 weeks. Plasma glucose, insulin and lipids were assessed (n = 25). Immunostainings were performed in liver, pancreas and fat (N = 10).…

0301 basic medicinemedicine.medical_specialtymedicine.medical_treatment030209 endocrinology & metabolismlcsh:TX341-641Carbohydrate metabolismtransgenic miceArticle03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineAdipocyteDiabetes mellitusHyperlipidemialipid metabolismmedicinecarbohydrate metabolismhigh-sucrose diethigh-fatNutrition and DieteticsCholesterolInsulinType 2 Diabetes MellituscholesterolLipid metabolismmedicine.diseaselipoproteins030104 developmental biologyEndocrinologychemistrylipids (amino acids peptides and proteins)atherosclerosissterol regulatory element-binding protein 2 (SREBP-2)lcsh:Nutrition. Foods and food supplyFood ScienceNutrients
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Genome-based in silico identification of new Mycobacterium tuberculosis antigens activating polyfunctional CD8+ T cells in human tuberculosis.

2011

Although CD8(+) T cells help control Mycobacterium tuberculosis infection, their M. tuberculosis Ag repertoire, in vivo frequency, and functionality in human tuberculosis (TB) remains largely undefined. We have performed genome-based bioinformatics searches to identify new M. tuberculosis epitopes presented by major HLA class I supertypes A2, A3, and B7 (covering 80% of the human population). A total of 432 M. tuberculosis peptides predicted to bind to HLA-A*0201, HLA-A*0301, and HLA-B*0702 (representing the above supertypes) were synthesized and HLA-binding affinities determined. Peptide-specific CD8(+) T cell proliferation assays (CFSE dilution) in 41 M. tuberculosis-responsive donors ide…

AdultIntracellular FluidMaleTuberculosisT cellImmunologyEpitopes T-LymphocyteHuman leukocyte antigenCD8-Positive T-LymphocytesLymphocyte ActivationEpitopeTuberculosis CD8 T cells cytokinesMycobacterium tuberculosis03 medical and health sciencesAntigenifn-gamma protective efficacy binding-affinity dormancy regulon subunit vaccine transgenic mice hla-b epitopes infection responsesPredictive Value of TestsmedicineImmunology and AllergyCytotoxic T cellHumansTuberculosis030304 developmental biologyAged0303 health sciencesAntigens Bacterialbiology030306 microbiologyGenome HumanComputational BiologyMycobacterium tuberculosisMiddle Agedbiology.organism_classificationmedicine.diseaseVirology3. Good healthmedicine.anatomical_structureFemaleCD8Genome BacterialJournal of immunology (Baltimore, Md. : 1950)
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Cluster-determinant 36 (CD36) impacts on vitamin E postprandial response

2014

International audience; Scope: A single nucleotide polymorphism in the cluster determinant 36 (CD36) gene has recently been associated with plasma alpha-tocopherol concentration, suggesting a possible role of this protein in vitamin E intestinal absorption or tissue uptake. Methods and results: To investigate the involvement of CD36 in vitamin E transport, we first evaluated the effect of CD36 on alpha- and gamma-tocopherol transmembrane uptake and efflux using transfected HEK cells. gamma-Tocopherol postprandial response was then assessed in CD36-deficient mice compared with wild-type mice, after the mice had been fully characterized for their alpha -tocopherol, vitamin A and lipid plasma,…

CD36 AntigensMaleGenetically modified mouseVitaminmedicine.medical_specialtyBioavailability[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionCD36medicine.medical_treatmentalpha-TocopherolBiologyPolymorphism Single NucleotideIntestinal absorptionMice03 medical and health scienceschemistry.chemical_compoundInternal medicinemedicineAnimalsHumansTransgenic miceVitamin ATriglyceridesComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesgamma-TocopherolIntestinal absorptionVitamin E030302 biochemistry & molecular biologyHypertriglyceridemiaLipid metabolismLipid MetabolismPostprandial Periodmedicine.disease[SDV.AEN] Life Sciences [q-bio]/Food and NutritionCholesterolHEK293 CellsEndocrinologyPostprandialLiverchemistrybiology.proteinFemalelipids (amino acids peptides and proteins)CD36[SDV.AEN]Life Sciences [q-bio]/Food and NutritionFood ScienceBiotechnologyMolecular Nutrition & Food Research
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Expression of genes encoding the calcium signalosome in cellular and transgenic models of Huntington's disease

2013

Huntington's disease (HD) is a hereditary neurodegenerative disease caused by the expansion of a polyglutamine stretch in the huntingtin (HTT) protein and characterized by dysregulated calcium homeostasis. We investigated whether these disturbances are correlated with changes in the mRNA level of the genes that encode proteins involved in calcium homeostasis and signaling (i.e., the calciosome). Using custom-made TaqMan low-density arrays containing probes for 96 genes, we quantified mRNA in the striatum in YAC128 mice, a model of HD, and wildtype mice. HTT mutation caused the increased expression of some components of the calcium signalosome, including calretinin, presenilin 2, and calmyri…

Huntingtinhuntingtincalcium signalosomechemistry.chemical_elementtransgenic miceCalciumlcsh:RC321-571Cellular and Molecular Neurosciencehuntingtin-associated protein 1mental disordersGene expressionOriginal Research Articlelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyCalcium metabolismTaqMan low-density arraysbiologyHuntingtin-associated protein 1Calcium channelTaqMan Low Density Arraysstore-operated calcium entrycalcyclin-binding proteinHuntington's diseaseMolecular biologyStore-operated calcium entrynervous systemchemistrybiology.proteinCalretininHuntington’s diseaseNeuroscienceFrontiers in Molecular Neuroscience
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A New Tool for the Analysis of the Effect of Intracerebrally Injected Anti-Amyloid-β Compounds

2021

Background: A wide range of techniques has been developed over the past decades to characterize amyloid-β (Aβ) pathology in mice. Until now, no method has been established to quantify spatial changes in Aβ plaque deposition due to targeted delivery of substances using ALZET® pumps. Objective: Development of a methodology to quantify the local distribution of Aβ plaques after intracerebral infusion of compounds. Methods: We have developed a toolbox to quantify Aβ plaques in relation to intracerebral injection channels using Zeiss AxioVision® and Microsoft Excel® software. For the proof of concept, intracerebral stereotactic surgery was performed in 50-day-old APP-transgenic mice injected wit…

Intracerebral injectionAmyloid βMice TransgenicPlaque Amyloidamyloid-βtransgenic miceStereotaxic TechniqueshistologyMiceAlzheimer DiseaseAnimalsHumansDistribution (pharmacology)implantable infusion pumpdistributional activityAmyloid beta-PeptidesChemistryGeneral NeuroscienceBrainGeneral MedicineImmunohistochemistryplaquesAβ depositionquantificationDisease Models AnimalPsychiatry and Mental healthClinical PsychologyGeriatrics and GerontologyAlzheimer’s diseaseResearch ArticleBiomedical engineeringJournal of Alzheimer's Disease
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Keratinocyte-Derived Granulocyte-Macrophage Colony Stimulating Factor Accelerates Wound Healing: Stimulation of Keratinocyte Proliferation, Granulati…

2001

Chronic, nonhealing wounds represent a major clinical challenge to practically all disciplines in modern medicine including dermatology, oncology, surgery, and hematology. In skin wounds, granulocyte-macrophage colony stimulating factor (GM-CSF) is secreted by keratinocytes shortly after injury and mediates epidermal cell proliferation in an autocrine manner. Many other cells involved in wound healing including macrophages, lymphocytes, fibroblasts, endothelial cells, and dendritic cells synthesize GM-CSF and/or are targets of this cytokine. Therefore, GM-CSF is a pleiotropic cytokine evoking complex processes during wound repair. Despite this complexity and the scarcity of mechanistic unde…

Macrophage colony-stimulating factorKeratinocytesMalemedicine.medical_treatmentGene ExpressionMitosisNeovascularization PhysiologicMice TransgenicDermatologytransgenic miceBiologyBiochemistryProinflammatory cytokineTransforming Growth Factor beta1MiceTransforming Growth Factor betamedicineAnimalsRNA MessengerAutocrine signallingMolecular BiologySkinWound Healingintegumentary systemGranulation tissueGranulocyte-Macrophage Colony-Stimulating FactorGM-CSFCell BiologyUp-RegulationCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorImmunologyModels AnimalCancer researchCarcinogensGranulation TissueCytokinesTetradecanoylphorbol AcetateFemaleKeratinocyteWound healingmedicine.drugJournal of Investigative Dermatology
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ApoB100,LDLR-/- mice exhibit reduced electroretinographic response and cholesteryl esters deposits in the retina

2008

International audience; PURPOSE. To evaluate the retinal phenotype of 7- and 14-month-old apoB100,LDLR–/– mice, a relevant animal model of lipid metabolism dysfunction. METHODS. Single-flash electroretinograms were obtained from 7- and 14-month-old apoB100,LDLR–/– and control mice fed a standard diet under both scotopic and photopic conditions. Visual cycle retinoids were analyzed in eyes from dark-adapted mice. Retinal and choroidal vascularization was evaluated with scanning laser ophthalmoscopy. Fatty acids were analyzed in the retina. Esterified and free cholesterol was detected in eye cryosections. RESULTS. Scotopic and photopic b-wave amplitudes were significantly reduced in apoB100,L…

MaleHUMAN BRUCHS MEMBRANEgenetic structuresHIGH-FAT DIETLipid Metabolism DisordersBasement MembraneAGE-RELATED MACULOPATHYchemistry.chemical_compoundMice0302 clinical medicine[SDV.IDA]Life Sciences [q-bio]/Food engineeringFluorescein AngiographyPigment Epithelium of EyeTRANSGENIC MICE0303 health sciencesmedicine.diagnostic_testROD OUTER SEGMENTSmedicine.anatomical_structureBiochemistryHUMAN APOLIPOPROTEIN-BApolipoprotein B-100Femalelipids (amino acids peptides and proteins)Cholesterol EstersPhotopic visionVisual phototransductionmedicine.medical_specialtyDark AdaptationMice TransgenicBiologyRetinaRECEPTOR-NEGATIVE MICE03 medical and health sciencesRetinoidsRetinal DiseasesBASAL DEPOSITSInternal medicinemedicineElectroretinographyAnimals[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringFilipinHUMAN ATHEROSCLEROTIC LESIONS030304 developmental biologyRetinaRetinal pigment epitheliumRetinalMacular degenerationmedicine.diseaseMACULAR DEGENERATIONeye diseasesMice Inbred C57BLOphthalmoscopyEndocrinologychemistryReceptors LDLLDL receptor030221 ophthalmology & optometrysense organsPhotic StimulationElectroretinography
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Abnormal accumulation of autophagic vesicles correlates with axonal and synaptic pathology in young Alzheimer's mice hippocampus

2012

Dystrophic neurites associated with amyloid plaques precede neuronal death and manifest early in Alzheimer's disease (AD). In this work we have characterized the plaque-associated neuritic pathology in the hippocampus of young (4- to 6-month-old) PS1(M146L)/APP(751SL) mice model, as the initial degenerative process underlying functional disturbance prior to neuronal loss. Neuritic plaques accounted for almost all fibrillar deposits and an axonal origin of the dystrophies was demonstrated. The early induction of autophagy pathology was evidenced by increased protein levels of the autophagosome marker LC3 that was localized in the axonal dystrophies, and by electron microscopic identification…

Pathologymedicine.medical_specialtyNeuriteClinical NeurologyHippocampusMice TransgenicPlaque AmyloidAmyloid plaquesBiologyHippocampal formationHippocampusDystrophic neuritesPathology and Forensic MedicineAmyloid beta-Protein PrecursorMiceCellular and Molecular NeuroscienceAlzheimer DiseaseAutophagyNeuritesmedicineElectron microscopyLC3AnimalsSenile plaquesMicroscopy ImmunoelectronNeuronsSynaptosomeOriginal PaperPS1/APP transgenic miceCytoplasmic VesiclesAutophagymedicine.diseaseAxonsDisease Models AnimalPresynaptic terminalsAxoplasmic transportNeurology (clinical)Alzheimer's disease
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Susceptibility to collagen-induced arthritis is modulated by TGFβ responsiveness of T cells

2004

The objective of our study was to determine the regulatory effects that endogenous transforming growth factor beta (TGFbeta) exerts on T cells in the pathogenesis of collagen-induced arthritis (CIA). CIA was induced in transgenic mice expressing a dominant negative TGFbeta type II receptor in T cells under the control of the human CD2 promoter. Clinical and histological arthritis scores were determined and experiments on disease induction and the healing phase of disease were performed. The proliferation and cytokine production of draining lymph node cells in vitro were analyzed. Transgenic mice were more susceptible to induction of CIA. The overall incidence was higher in transgenic mice t…

T-LymphocytesMice Inbred StrainsMice Transgenictransgenic miceTh1 CellsArthritis ExperimentalSeverity of Illness Indexdominant negative TGFβ type II receptorArthritis RheumatoidMiceMice Inbred DBATransforming Growth Factor betaAnimalsCytokinesCattleDisease SusceptibilityLymph NodesCollagen Type IICells CulturedCrosses GeneticResearch ArticleIFNγCell ProliferationArthritis Research & Therapy
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