Search results for " Transgenic"

showing 10 items of 522 documents

Predominant pathogenic role of tumor necrosis factor in experimental colitis in mice

1997

Antibodies to tumor necrosis factor (TNF)-alpha have been recently proposed as effective treatment for patients with Crohn's disease. Here, we analyze the functional role of TNF-alpha in a mouse model of chronic intestinal inflammation induced by the hapten reagent 2,4,6,-trinitrobenzene sulfonic acid (TNBS) that mimics some characteristics of Crohn's disease in humans. Macrophage-enriched lamina propria (LP) mononuclear cells from mice with TNBS-induced colitis produced 10-30-fold higher levels of TNF-alpha mRNA and protein than cells from control mice. When mice with chronic colitis were treated by intraperitoneal injection of antibodies to TNF-alpha, an improvement of both the clinical a…

PancolitisImmunologyMice Inbred StrainsMice TransgenicInflammationInflammatory bowel diseaseAntibodiesMicemedicineAnimalsImmunology and AllergyColitisMice KnockoutLamina propriaCrohn's diseaseTumor Necrosis Factor-alphabusiness.industryInterleukinColitisInflammatory Bowel Diseasesmedicine.diseaseDisease Models Animalmedicine.anatomical_structureTrinitrobenzenesulfonic AcidChronic DiseaseImmunologyFemaleTumor necrosis factor alphamedicine.symptombusinessEuropean Journal of Immunology
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Synaptopodin regulates denervation-induced homeostatic synaptic plasticity

2013

Synaptopodin (SP) is a marker and essential component of the spine apparatus (SA), an enigmatic cellular organelle composed of stacked smooth endoplasmic reticulum that has been linked to synaptic plasticity. However, SP/SA-mediated synaptic plasticity remains incompletely understood. To study the role of SP/SA in homeostatic synaptic plasticity we here used denervation-induced synaptic scaling of mouse dentate granule cells as a model system. This form of plasticity is of considerable interest in the context of neurological diseases that are associated with the loss of neurons and subsequent denervation of connected brain regions. In entorhino-hippocampal slice cultures prepared from SP-de…

Patch-Clamp TechniquesDendritic SpinesGreen Fluorescent ProteinsNonsynaptic plasticityMice TransgenicTetrodotoxinBiologyIn Vitro TechniquesHippocampusReceptors N-Methyl-D-AspartateMiceHomeostatic plasticitySynaptic augmentationMetaplasticityAnimalsEntorhinal CortexHomeostasisPromoter Regions GeneticMultidisciplinarySynaptic scalingNeuronal PlasticityMicrofilament ProteinsRyanodine Receptor Calcium Release ChannelBiological SciencesDenervationSpine apparatusMice Inbred C57BLSynaptic fatigueSynaptic plasticityDentate GyrusSynapsesCalcium ChannelsNeuroscience
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A subset of ventral tegmental area dopamine neurons responds to acute ethanol

2015

The mechanisms by which alcohol drinking promotes addiction in humans and self-administration in rodents remain obscure, but it is well known that alcohol can enhance dopamine (DA) neurotransmission from neurons of the ventral tegmental area (VTA) and increase DA levels within the nucleus accumbens and prefrontal cortex. We recorded from identified DA neuronal cell bodies within ventral midbrain slices prepared from a transgenic mouse line (TH-GFP) using long-term stable extracellular recordings in a variety of locations and carefully mapped the responses to applied ethanol (EtOH). We identified a subset of DA neurons in the medial VTA located within the rostral linear and interfascicular n…

Patch-Clamp TechniquesGreen Fluorescent ProteinsAction PotentialsMice TransgenicNucleus accumbensNeurotransmissionArticleTissue Culture TechniquesMidbrainQuinpiroleDopamineDopamine receptor D2mental disordersmedicineAnimalsDose-Response Relationship DrugEthanolChemistryDopaminergic NeuronsGeneral NeuroscienceVentral Tegmental AreaCentral Nervous System DepressantsMice Inbred C57BLVentral tegmental areamedicine.anatomical_structurenervous systemNeuronNeurosciencemedicine.drugNeuroscience
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Perlecan is critical for heart stability

2008

Aims Perlecan is a heparansulfate proteoglycan found in basement membranes, cartilage, and several mesenchymal tissues that form during development, tumour growth, and tissue repair. Loss-of-function mutations in the perlecan gene in mice are associated with embryonic lethality caused primarily by cardiac abnormalities probably due to hemopericards. The aim of the present study was to investigate the mechanism underlying the early embryonic lethality and the pathophysiological relevance of perlecan for heart function. Methods and results Perlecan-deficient murine embryonic stem cells were used to investigate the myofibrillar network and the electrophysiological properties of single cardiomy…

Patch-Clamp TechniquesPhysiologyMyocardial InfarctionMice TransgenicCell CommunicationPerlecanSarcomereBasement MembraneVentricular Function LeftAdherens junctionExtracellular matrixMicePhysiology (medical)medicineAnimalsMyocytes CardiacCells CulturedEmbryonic Stem CellsBasement membranebiologyCartilageCell DifferentiationHeartAnatomyEmbryonic stem cellCell biologyMice Inbred C57BLcarbohydrates (lipids)Disease Models Animalmedicine.anatomical_structurebiology.proteinFemaleCardiology and Cardiovascular MedicineMyofibrilHeparan Sulfate ProteoglycansCardiovascular Research
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“Super p53” Mice Display Retinal Astroglial Changes

2013

Tumour-suppressor genes, such as the p53 gene, produce proteins that inhibit cell division under adverse conditions, as in the case of DNA damage, radiation, hypoxia, or oxidative stress (OS). The p53 gene can arrest proliferation and trigger death by apoptosis subsequent to several factors. In astrocytes, p53 promotes cell-cycle arrest and is involved in oxidative stress-mediated astrocyte cell death. Increasingly, astrocytic p53 is proving fundamental in orchestrating neurodegenerative disease pathogenesis. In terms of ocular disease, p53 may play a role in hypoxia due to ischaemia and may be involved in the retinal response to oxidative stress (OS). We studied the influence of the p53 ge…

PathologyAnatomy and PhysiologyCell divisionMouselcsh:MedicineFluorescent Antibody Techniquemedicine.disease_causechemistry.chemical_compoundMiceMolecular Cell Biologylcsh:ScienceMultidisciplinaryGlial fibrillary acidic proteinAnimal ModelsCell biologymedicine.anatomical_structureMedicineOftalmologíaDNA modificationAstrocyteResearch ArticleSignal TransductionProgrammed cell deathmedicine.medical_specialtyCell PhysiologyHistologyOcular AnatomyNeurocienciasMice TransgenicBiologyRetinaModel OrganismsOcular SystemGlial Fibrillary Acidic ProteinmedicineGeneticsAnimalsBiologyRetinaStaining and Labelinglcsh:RRetinalAnatomía ocularMice Inbred C57BLGenética médicaOphthalmologychemistryApoptosisAstrocytesbiology.proteinlcsh:QGene expressionGene FunctionTumor Suppressor Protein p53Animal GeneticsOxidative stress
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Cutting edge: Multiple sclerosis-like lesions induced by effector CD8 T cells recognizing a sequestered antigen on oligodendrocytes.

2008

Abstract CD8 T cells are emerging as important players in multiple sclerosis (MS) pathogenesis, although their direct contribution to tissue damage is still debated. To assess whether autoreactive CD8 T cells can contribute to the pronounced loss of oligodendrocytes observed in MS plaques, we generated mice in which the model Ag influenza hemagglutinin is selectively expressed in oligodendrocytes. Transfer of preactivated hemagglutinin-specific CD8 T cells led to inflammatory lesions in the optic nerve, spinal cord, and brain. These lesions, associating CD8 T cell infiltration with focal loss of oligodendrocytes, demyelination, and microglia activation, were very reminiscent of active MS le…

Pathologymedicine.medical_specialtyMultiple SclerosisImmunologyMice TransgenicBiologyCD8-Positive T-LymphocytesPathogenesisMiceAntigenmedicineImmunology and AllergyCytotoxic T cellAnimalsAntigensMyelin SheathMicrogliaMultiple sclerosismedicine.diseaseOligodendrocyteCell biologyOligodendrogliamedicine.anatomical_structureHemagglutininsOptic nerveInfiltration (medical)Journal of immunology (Baltimore, Md. : 1950)
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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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KLEIP Deficiency in Mice Causes Progressive Corneal Neovascular Dystrophy

2012

PURPOSE. The BTB-kelch protein KLEIP/KLHL20 is an actin binding protein that regulates cell-cell contact formation and cell migration. The aim of our study was to characterize KLEIP’s function in ocular health and disease in mice. METHODS. KLEIP -/- mice were generated, and corneas were examined histologically and stained for keratin-1, loricrin, keratin-12, keratin-14, CD31, LYVE-1, F4/80, E-cadherin, and Ki67. Corneal abrasions were performed after eyelid opening. RESULTS. Corneas of KLEIP þ/þ and KLEIP -/- mice were indistinguishable at birth. After eyelid opening corneal epithelial hyperplasia started to manifest in KLEIP -/- mice, showing a progressive epithelial metaplasia leading to …

Pathologymedicine.medical_specialtyStromal cellGenotypeMice TransgenicCorneal dystrophyReal-Time Polymerase Chain ReactionCorneaMiceCorneal OpacityCorneamedicineAnimalsCorneal NeovascularizationRNA MessengerAdaptor Proteins Signal TransducingCorneal epitheliumintegumentary systembusiness.industryDystrophymedicine.diseaseeye diseasesEpitheliumMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureGene Expression RegulationDisease ProgressionEpithelial MetaplasiaLoricrinsense organsCarrier ProteinsbusinessInvestigative Opthalmology & Visual Science
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Compromised central tolerance of ICA69 induces multiple organ autoimmunity

2014

For reasons not fully understood, patients with an organ-specific autoimmune disease have increased risks of developing autoimmune responses against other organs/tissues. We identified ICA69, a known β-cell autoantigen in Type 1 diabetes, as a potential common target in multi-organ autoimmunity. NOD mice immunized with ICA69 polypeptides exhibited exacerbated inflammation not only in the islets, but also in the salivary glands. To further investigate ICA69 autoimmunity, two genetically modified mouse lines were generated to modulate thymic ICA69 expression: the heterozygous ICA69(del/wt) line and the thymic medullary epithelial cell-specific deletion Aire-ΔICA69 line. Suboptimal central neg…

Primary Sjogren's syndromeGenetically modified mouseImmunologyThyroid GlandAutoimmune diabeteMice TransgenicThymus GlandBiologymedicine.disease_causeAutoantigensArticleSalivary GlandsSettore MED/13 - EndocrinologiaAutoimmune DiseasesAutoimmunityImmune toleranceAutoimmune thyroiditisIslets of LangerhansMiceICA69Mice Inbred NODImmune TolerancemedicineAnimalsImmunology and AllergyThymuAutoimmune thyroiditiNOD miceInflammationAutoimmune diseaseStomachmedicine.diseaseGene Expression RegulationAutoimmune polyendocrine syndromeImmunologyAutoimmune polyendocrine syndromeCentral toleranceJournal of Autoimmunity
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De Novo prion aggregates trigger autophagy in skeletal muscle

2014

ABSTRACT In certain sporadic, familial, and infectious prion diseases, the prion protein misfolds and aggregates in skeletal muscle in addition to the brain and spinal cord. In myocytes, prion aggregates accumulate intracellularly, yet little is known about clearance pathways. Here we investigated the clearance of prion aggregates in muscle of transgenic mice that develop prion disease de novo . In addition to neurodegeneration, aged mice developed a degenerative myopathy, with scattered myocytes containing ubiquitinated, intracellular prion inclusions that were adjacent to myocytes lacking inclusions. Myocytes also showed elevated levels of the endoplasmic reticulum chaperone Grp78/BiP, su…

PrionsAutophagosome maturationanimal diseasesBlotting WesternImmunologyMice TransgenicBiologyProtein degradationPolymerase Chain ReactionMedical and Health SciencesMicrobiologyTransgenicPrion DiseasesMiceVirologyAutophagymedicineAnimalsMyocyteMuscle SkeletalEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsDNA PrimersMuscle CellsAgricultural and Veterinary SciencesBlottingEndoplasmic reticulumNeurodegenerationAutophagySkeletal muscleSkeletalBiological Sciencesmedicine.diseaseImmunohistochemistryMolecular biologynervous system diseasesmedicine.anatomical_structureInsect ScienceChaperone (protein)biology.proteinMuscleWestern
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