Search results for " Transgenic"

showing 10 items of 522 documents

Brain erythropoietin fine-tunes a counterbalance between neurodifferentiation and microglia in the adult hippocampus

2021

In adult cornu ammonis hippocampi, erythropoietin (EPO) expression drives the differentiation of new neurons,independent of DNA synthesis, and increases dendritic spine density. This substantial brain hardwareupgrade is part of a regulatory circle: during motor-cognitive challenge, neurons experience ‘‘functional’’hypoxia, triggering neuronal EPO production, which in turn promotes improved performance. Here, weshow an unexpected involvement of resident microglia. During EPO upregulation and stimulated neurodifferentiation,either by functional or inspiratory hypoxia, microglia numbers decrease. Treating mice with recombinanthuman (rh)EPO or exposure to hypoxia recapitulates these changes and…

Dendritic spineQH301-705.5Mice TransgenicBiologyHippocampusGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationrecombinant human EPOhemic and lymphatic diseasesmedicineAnimalsBiology (General)Hypoxia BrainReceptorErythropoietin030304 developmental biology0303 health sciencesMicrogliahypoxiaPyramidal CellsNeurogenesisneurodifferentiationCell DifferentiationHypoxia (medical)CSF1Rneurogenesismedicine.anatomical_structurenervous systemErythropoietinApoptosisIL-34Microgliamedicine.symptomNeuroscience030217 neurology & neurosurgerymedicine.drug
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Cellular Plasticity in the Adult Murine Piriform Cortex: Continuous Maturation of Dormant Precursors Into Excitatory Neurons

2017

Neurogenesis in the healthy adult murine brain is based on proliferation and integration of stem/progenitor cells and is thought to be restricted to 2 neurogenic niches: the subventricular zone and the dentate gyrus. Intriguingly, cells expressing the immature neuronal marker doublecortin (DCX) and the polysialylated-neural cell adhesion molecule reside in layer II of the piriform cortex. Apparently, these cells progressively disappear along the course of ageing, while their fate and function remain unclear. Using DCX-CreERT2/Flox-EGFP transgenic mice, we demonstrate that these immature neurons located in the murine piriform cortex do not vanish in the course of aging, but progressively res…

Doublecortin Domain Proteins0301 basic medicineDoublecortin ProteinCognitive NeuroscienceCell PlasticityGreen Fluorescent ProteinsSubventricular zoneMice TransgenicNerve Tissue ProteinsNeural Cell Adhesion Molecule L1Piriform CortexBiologyMice03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineCortex (anatomy)Piriform cortexNeuroplasticitymedicineAnimalsNeuronsGlutamate DecarboxylaseStem CellsDentate gyrusNeuropeptidesNeurogenesisGene Expression Regulation DevelopmentalEmbryo MammalianCell biologyDoublecortinMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureBromodeoxyuridinenervous systemSialic Acidsbiology.proteinTBR1Calcium-Calmodulin-Dependent Protein Kinase Type 2Microtubule-Associated Proteins030217 neurology & neurosurgeryCerebral Cortex
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Dual roles of Aβ in proliferative processes in an amyloidogenic model of Alzheimer’s disease

2017

Alzheimer’s disease is a major neurodegenerative disorder that leads to severe cognitive deficits in the elderly population. Over the past two decades, multiple studies have focused on elucidating the causative factors underlying memory defects in Alzheimer’s patients. In this regard, new evidence linking Alzheimer’s disease-related pathology and neuronal stem cells suggests that hippocampal neurogenesis impairment is an important factor underlying these cognitive deficits. However, because of conflicting results, the impact of Aβ pathology on neurogenesis/gliogenesis remains unclear. Here, we investigated the effect of Aβ on neuronal and glial proliferation by using an APP/PS1 transgenic m…

Doublecortin Domain ProteinsMale0301 basic medicineCellular pathologyPathologymedicine.medical_specialtyNeurogenesisGene ExpressionHippocampuslcsh:MedicineMice TransgenicBiologyHippocampusArticleAmyloid beta-Protein PrecursorMice03 medical and health sciences0302 clinical medicineNeural Stem CellsAlzheimer DiseaseSpheroids CellularNeurospheremedicineAnimalsHumansProgenitor celllcsh:ScienceCells CulturedCell ProliferationGliogenesisNeuronsAmyloid beta-PeptidesMultidisciplinaryNeuropeptidesNeurogenesislcsh:RCell DifferentiationNeural stem cellDisease Models Animal030104 developmental biologynervous systemOrgan Specificitylcsh:QStem cellMicrotubule-Associated ProteinsNeurogliaNeuroscience030217 neurology & neurosurgery
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Functional Integration of Neuronal Precursors in the Adult Murine Piriform Cortex

2018

Abstract The extent of functional maturation and integration of nonproliferative neuronal precursors, becoming neurons in the adult murine piriform cortex, is largely unexplored. We thus questioned whether precursors eventually become equivalent to neighboring principal neurons or whether they represent a novel functional network element. Adult brain neuronal precursors and immature neurons (complex cells) were labeled in transgenic mice (DCX-DsRed and DCX-CreERT2 /flox-EGFP), and their cell fate was characterized with patch clamp experiments and morphometric analysis of axon initial segments. Young (DCX+) complex cells in the piriform cortex of 2- to 4-month-old mice received sparse synapt…

Doublecortin ProteinNeurogenesisCognitive NeuroscienceMice TransgenicPiriform CortexBiologyCell fate determinationtangled cellsaxon initial segmentMiceCellular and Molecular NeuroscienceNeural Stem CellsdoublecortinPiriform cortexmedicineAnimalsPatch clampNeuronsNeuropeptidesNeurogenesisGene Expression Regulation DevelopmentalCell Differentiationcomplex cellsAxon initial segmentDoublecortinadult neurogenesismedicine.anatomical_structurenervous systembiology.proteinGABAergicOriginal ArticleNeuronMicrotubule-Associated ProteinsNeuroscienceCerebral Cortex
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Polymer-doxycycline conjugates as fibril disrupters: an approach towards the treatment of a rare amyloidotic disease.

2014

The term amyloidosis describes neurological diseases where an abnormal protein is misfolded and accumulated as deposits in organs and tissues, known as amyloid, disrupting their normal function. In the most common familial amyloid polyneuropathy (FAP), transthyretin (TTR) displays this role primarily affecting the peripheral nervous system (PNS). Advanced stages of this inherited rare amyloidosis, present as fibril deposits that are responsible for disease progression. In order to stop disease progression, herein we designed an efficient family of nanoconjugates as fibril disrupters. These polymer conjugates are based on doxycycline (doxy), already in phase II trials for Alzheimer's disease…

DrugAmyloidErythrocytesAmyloidmedia_common.quotation_subjectPharmaceutical ScienceMice TransgenicFibrilHemolysisPlasmaIn vivomedicinePolymeric drugAnimalsTissue DistributionAmyloid disruptersmedia_commonDoxycyclineAmyloid Neuropathies FamilialMice Inbred BALB CbiologyChemistryAmyloidosismedicine.diseaseRare diseasesRatsTransthyretinPolymer-drug conjugateDisease Models AnimalDrug LiberationBiochemistryPolyglutamic AcidDoxycyclineDrug deliveryDrug deliverybiology.proteinCancer researchPolymer therapeuticsmedicine.drugJournal of controlled release : official journal of the Controlled Release Society
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MAPK3 deficiency drives autoimmunity via DC arming.

2010

DC are professional APC that instruct T cells during the inflammatory course of EAE. We have previously shown that MAPK3 (Erk1) is important for the induction of T-cell anergy. Our goal was to determine the influence of MAPK3 on the capacity of DC to arm T-cell responses in autoimmunity. We report that DC from Mapk3(-/-) mice have a significantly higher membrane expression of CD86 and MHC-II and--when loaded with the myelin oligodendrocyte glycoprotein--show a superior capacity to prime naive T cells towards an inflammatory phenotype than Mapk3(+/+) DC. Nonetheless and as previously described, Mapk3(-/-) mice were only slightly but not significantly more susceptible to myelin oligodendrocyt…

Encephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemOvalbuminImmunologyMedizinAutoimmunityMice TransgenicT-Cell Antigen Receptor SpecificityBiologymedicine.disease_causeAutoimmunityMyelinMiceImmune systemT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsNeuroinflammationGlycoproteinsCD86Mitogen-Activated Protein Kinase 3KinaseHistocompatibility Antigens Class IIDendritic Cellsmedicine.diseaseOligodendrocytePeptide FragmentsSpecific Pathogen-Free OrganismsMice Inbred C57BLmedicine.anatomical_structureRadiation ChimeraImmunologyCytokinesMyelin-Oligodendrocyte GlycoproteinB7-2 AntigenInfiltration (medical)European journal of immunology
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Animal models of Multiple Sclerosis

2015

Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) which involves a complex interaction between immune system and neural cells. Animal modeling has been critical for addressing MS pathogenesis. The three most characterized animal models of MS are (1) the experimental autoimmune/allergic encephalomyelitis (EAE); (2) the virally-induced chronic demyelinating disease, known as Theiler׳s murine encephalomyelitis virus (TMEV) infection and (3) the toxin-induced demyelination. All these models, in a complementary way, have allowed to reach a good knowledge of the pathogenesis of MS. Specifically, EAE is the model which better reflects the autoimmu…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisCentral nervous systemMice TransgenicArticlePathogenesisMice03 medical and health sciences0302 clinical medicineImmune systemTheilovirusCardiovirus InfectionsmedicineDemyelinating diseaseAnimalsHumansRemyelination030304 developmental biologyPharmacology0303 health sciencesbusiness.industryEAEMultiple sclerosisAllergic Encephalomyelitismedicine.disease3. Good healthDisease Models AnimalInflammatory demyelinating diseasemedicine.anatomical_structureImmune systemImmunologyEAE; Immune system; Multiple SclerosisbusinessNeuroscience030217 neurology & neurosurgery
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Primary oligodendrocyte death does not elicit anti-CNS immunity.

2012

Anti-myelin immunity is commonly thought to drive multiple sclerosis, yet the initial trigger of this autoreactivity remains elusive. One of the proposed factors for initiating this disease is the primary death of oligodendrocytes. To specifically test such oligodendrocyte death as a trigger for anti-CNS immunity, we inducibly killed oligodendrocytes in an in vivo mouse model. Strong microglia-macrophage activation followed oligodendrocyte death, and myelin components in draining lymph nodes made CNS antigens available to lymphocytes. However, even conditions favoring autoimmunity-bystander activation, removal of regulatory T cells, presence of myelin-reactive T cells and application of dem…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisEncephalomyelitisTransgene610 Medicine & healthMice TransgenicBiology10263 Institute of Experimental Immunology03 medical and health sciencesMyelinMice0302 clinical medicineAntigenImmunitymedicineAnimalsGene Knock-In TechniquesCells Cultured030304 developmental biology0303 health sciencesCell DeathGeneral NeuroscienceMultiple sclerosis2800 General Neurosciencemedicine.diseaseOligodendrocyteOligodendrogliamedicine.anatomical_structureImmunology570 Life sciences; biologyExperimental pathologyNeuroscience030217 neurology & neurosurgeryNature neuroscience
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Smad7 in T cells drives T helper 1 responses in multiple sclerosis and experimental autoimmune encephalomyelitis

2010

Autoreactive CD4+ T lymphocytes play a vital role in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis. Since the discovery of T helper 17 cells, there is an ongoing debate whether T helper 1, T helper 17 or both subtypes of T lymphocytes are important for the initiation of autoimmune neuroinflammation. We examined peripheral blood CD4+ cells from patients with active and stable relapsing-remitting multiple sclerosis, and used mice with conditional deletion or over-expression of the transforming growth factor-beta inhibitor Smad7, to delineate the role of Smad7 in T cell differentiation and autoimmune neuroinflammation. We found that Smad…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisT helper 1Regulatory T cellT cellMolecular Sequence DataMice TransgenicBiologySmad7 ProteinMiceInterleukin 21medicineAnimalsHumansCytotoxic T cellAmino Acid SequenceIL-2 receptorAntigen-presenting cellMice Knockoutintegumentary systemEAEimmune regulationCD28Original ArticlesTh1 CellsNatural killer T cellMice Inbred C57BLmedicine.anatomical_structureT cell responsesImmunologyNeurology (clinical)Brain
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Myelin-specific T cells also recognize neuronal autoantigen in a transgenic mouse model of multiple sclerosis

2008

T-cell recognition of autoantigens is important in the development of autoimmune disease. Now, Hartmut Wekerle and his colleagues demonstrate that organ-specific autoimmune responses may be driven by T cells that simultaneously respond to two different autoantigens found within the same target tissue. We describe here the paradoxical development of spontaneous experimental autoimmune encephalomyelitis (EAE) in transgenic mice expressing a myelin oligodendrocyte glycoprotein (MOG)-specific T cell antigen receptor (TCR) in the absence of MOG. We report that in Mog-deficient mice (Mog−/−), the autoimmune response by transgenic T cells is redirected to a neuronal cytoskeletal self antigen, neur…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisT-LymphocytesMolecular Sequence DataReceptors Antigen T-CellMice TransgenicCross ReactionsMajor histocompatibility complexAutoantigensGeneral Biochemistry Genetics and Molecular BiologyEpitopeMyelin oligodendrocyte glycoproteinMice03 medical and health sciencesMyelin0302 clinical medicineAntigenNeurofilament ProteinsAnimalsMedicineAmino Acid SequenceMyelin Sheath030304 developmental biologyAutoimmune disease0303 health sciencesbiologybusiness.industryExperimental autoimmune encephalomyelitisT-cell receptorGeneral Medicinemedicine.disease3. Good healthMice Inbred C57BLDisease Models AnimalMyelin-Associated Glycoproteinmedicine.anatomical_structureImmunologybiology.proteinMyelin-Oligodendrocyte GlycoproteinbusinessMyelin Proteins030215 immunologyNature Medicine
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