Search results for " mouse"

showing 10 items of 343 documents

2014

Background While the immune pathogenesis caused by hepatitis B virus (HBV) infection has been studied extensively, little is known about direct pathogenic effects of HBV surface proteins. Here, we have investigated pathological cellular effects of HBV surface protein expression in the liver of transgenic mice with different genetic background.

Genetically modified mouseHepatitis B virusRegulation of gene expressionMultidisciplinaryTransgenevirus diseasesHepatitis BBiologymedicine.disease_causemedicine.diseasedigestive system diseasesFibrosisImmunologySTAT proteinmedicineSignal transductionPLOS ONE
researchProduct

Abnormal development of pacinian corpuscles in double trkB;trkC knockout mice.

2006

Pacinian corpuscles depend on either Aalpha or Abeta nerve fibers of the large- and intermediate-sized sensory neurons for the development and maintenance of the structural integrity. These neurons express TrkB and TrkC, two members of the family of signal transducing neurotrophin receptors, and mice lacking TrkB and TrkC lost specific neurons and the sensory corpuscles connected to them. The impact of single or double targeted mutations in trkB and trkC genes in the development of Pacinian corpuscles was investigated in 25-day-old mice using immunohistochemistry and ultrastructural techniques. Single mutations on trkB or trkC genes were without effect on the structure and S100 protein expr…

medicine.medical_specialtyanimal structuresTropomyosin receptor kinase BBiologyTropomyosin receptor kinase CS100 proteinMiceMicroscopy Electron TransmissionInternal medicinemedicineLow-affinity nerve growth factor receptorAnimalsReceptor trkBReceptor trkCReceptorMice Knockoutmusculoskeletal neural and ocular physiologyGeneral NeuroscienceImmunohistochemistryCell biologyMice Inbred C57BLEndocrinologynervous systemAnimals NewbornTrk receptorembryonic structuresKnockout mousebiology.proteinPacinian CorpusclesNeurotrophinNeuroscience letters
researchProduct

Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
researchProduct

Preclinical xenograft models of human sarcoma show nonrandom loss of aberrations

2011

BACKGROUND: Human tumors transplanted into immunodeficient mice (xenografts) are good preclinical models, and it is important to identify possible systematic changes during establishment and passaging in mice. METHODS: High-resolution microarray-based comparative genomic hybridization (array CGH) was used to investigate how well a series of sarcoma xenografts, including 9 patient/xenograft pairs and 8 early versus late xenograft passage pairs, represented the patient tumor from which they originated. RESULTS: In all analyses, the xenografts were more similar to their tumor of origin than other xenografts of the same type. Most changes in aberration patterns were toward a more normal genome …

Cancer ResearchPathologymedicine.medical_specialtyMicroarraybiologyCancerPDGFRAbiology.organism_classificationmedicine.diseaseTransplantationNude mouseOncologyTumor progressionmedicineSarcomaComparative genomic hybridizationCancer
researchProduct

Membrane vesicles containing matrix metalloproteinase-9 and fibroblast growth factor-2 are released into the extracellular space from mouse mesoangio…

2010

Certain proteins, including fibroblast growth factor-2 (FGF-2) and matrix metalloproteinase-9 (MMP-9), have proved very effective in increasing the efficacy of mesoangioblast stem cell therapy in repairing damaged tissue. We provide the first evidence that mouse mesoangioblast stem cells release FGF-2 and MMP-9 in their active form through the production of membrane vesicles. These vesicles are produced and turned over continuously, but are stable for some time in the extracellular milieu. Mesoangioblasts shed membrane vesicles even under oxygen tensions that are lower than those typically used for cell culture and more like those of mouse tissues. These findings suggest that mesoangioblast…

ProteomicsTime FactorsPhysiologyClinical BiochemistryBiologyFibroblast growth factorCell LineMiceMembrane MicrodomainsTubulinParacrine CommunicationmedicineExtracellularAnimalsSecretionSettore BIO/06 - Anatomia Comparata E CitologiaFibroblastCytoskeletonMembrane vesicles MMP9 FGF2 mouse mesoangioblastMesoangioblastSecretory VesiclesVesicleBiological TransportMesenchymal Stem CellsCell BiologyCell biologyOxygenmedicine.anatomical_structureMatrix Metalloproteinase 9Cell cultureFibroblast Growth Factor 2Stem cellExtracellular Space
researchProduct

Improved models for animal research

2008

Experimental animal models are critical to understand gene function and human disease. Many rodent models are presently available providing avenues to elucidate gene function and/or to recapitulate specific pathological conditions. To a large extent, successful translation of clinical evidence or analytical data into appropriate mouse models is possible through progress in transgenic or gene deletion technology. Despite these significant improvements, major limitations still exist in manipulating the mouse genome. For this reason and to maximize success, the design and planning of mouse models need good knowledge concerning the requirements and limitations of commonly used strategies and em…

Genetically modified mouseHuman diseaseEmerging technologiesComputer sciencemedia_common.quotation_subjectKnockout mouseExperimental Animal ModelsComputational biologyFunction (engineering)GenomeFunctional genomicsmedia_common
researchProduct

Genome-wide meta-analyses of multiancestry cohorts identify multiple new susceptibility loci for refractive error and myopia

2013

Author version made available in accordance with the publisher's policy.

Candidate geneRefractive errorBone Morphogenetic Protein 2Genome-wide association studyVARIANTSGenomeGenome-wide association studies0302 clinical medicineRisk FactorsMyopiaGRIA4Genetics0303 health sciencesKCNQ Potassium ChannelsDisease geneticsEYE GROWTHASSOCIATIONRETINAL-PIGMENT EPITHELIUMRefractive ErrorsGenetic load3. Good healthADAPTED MOUSE RETINAMeta-analysisACIDPOTASSIUM CHANNELEXPRESSIONSingle-nucleotide polymorphismBiologyWhite PeopleArticle03 medical and health sciencesAsian PeoplemedicineGeneticsHumansGenetic Predisposition to DiseaseReceptors AMPAgene; myopia; refractive030304 developmental biologyHomeodomain Proteinsta1184ta3121medicine.diseaseGENEAlcohol OxidoreductasesSERINE-PROTEASEbiology.protein030221 ophthalmology & optometrySusceptibility locusTrans-ActivatorsEye disorderLamininSerine ProteasesGWAS; meta-analyses; refractive error; myopiaGenome-Wide Association StudyNature Genetics
researchProduct

Aβ and tau toxicities in Alzheimer’s are linked via oxidative stress-induced p38 activation: Protective role of vitamin E

2014

AbstractOxidative stress is a hallmark of Alzheimer’s disease (AD). We propose that rather than causing damage because of the action of free radicals, oxidative stress deranges signaling pathways leading to tau hyperphosphorylation, a hallmark of the disease. Indeed, incubation of neurons in culture with 5 µM beta-amyloid peptide (Aβ) causes an activation of p38 MAPK (p38) that leads to tau hyperphosphorylation. Inhibition of p38 prevents Aβ-induced tau phosphorylation. Aβ-induced effects are prevented when neurons are co-incubated with trolox (the water-soluble analog of vitamin E).We have confirmed these results in vivo, in APP/PS1 double transgenic mice of AD. We have found that APP/PS1 …

Genetically modified mouseMalemedicine.medical_specialtyCell signalingAntioxidantP-p38p38 mitogen-activated protein kinasesmedicine.medical_treatmentClinical BiochemistryMice Transgenictau ProteinsBiologyBeta-amyloidmedicine.disease_causeProtective AgentsBiochemistryHippocampusp38 Mitogen-Activated Protein KinasesArticlechemistry.chemical_compoundMiceAlzheimer DiseaseInternal medicinemental disordersmedicineVitamin EAnimalsPhosphorylationlcsh:QH301-705.5Cells CulturedNeuronslcsh:R5-920Amyloid beta-PeptidesVitamin EOrganic Chemistrymedicine.diseaseRatsDisease Models AnimalOxidative StressEndocrinologylcsh:Biology (General)chemistryTroloxAlzheimer's diseaseAntioxidantlcsh:Medicine (General)Oxidative stressRedox Biology
researchProduct

Wnt-Dependent Oligodendroglial-Endothelial Interactions Regulate White Matter Vascularization and Attenuate Injury

2020

Recent studies have indicated oligodendroglial-vascular crosstalk during brain development, but the underlying mechanisms are incompletely understood. We report that oligodendrocyte precursor cells (OPCs) contact sprouting endothelial tip cells in mouse, ferret and human neonatal white matter. Using transgenic mice, we show that increased or decreased OPC density results in cognate changes in white matter vascular investment. Hypoxia promoted both increased OPC numbers and higher white matter vessel density, and endothelial cell expression of the Wnt pathway targets Apcdd1 and Axin2, suggesting paracrine OPC-endothelial signaling. Conditional knockout of OPC Wntless resulted in diminished w…

0301 basic medicineGenetically modified mouseoligodendrocytesMice TransgenicBiologyArticleWhite matter03 medical and health sciencesParacrine signallingMice0302 clinical medicinetip cell angiogenesisAxin ProteinConditional gene knockoutmedicineAXIN2AnimalsHumanshypoxic-ischemic encephalopathyHypoxiaWnt Signaling PathwayGeneral NeuroscienceWnt signaling pathwayFerretsIntracellular Signaling Peptides and ProteinsEndothelial CellsMembrane ProteinsCell DifferentiationHypoxia (medical)Wnt signalingWhite Matter3. Good healthCell biologyEndothelial stem cellstomatognathic diseasesOligodendroglia030104 developmental biologymedicine.anatomical_structurenervous systemEndothelium Vascularmedicine.symptom030217 neurology & neurosurgeryNeuron
researchProduct

TGF-beta regulates airway responses via T cells.

2003

Abstract Allergic asthma is characterized by airway hyperreactivity, inflammation, and a Th2-type cytokine profile favoring IgE production. Beneficial effects of TGF-β and conflicting results regarding the role of Th1 cytokines have been reported from murine asthma models. In this study, we examined the T cell as a target cell of TGF-β-mediated immune regulation in a mouse model of asthma. We demonstrate that impairment of TGF-β signaling in T cells of transgenic mice expressing a dominant-negative TGF-β type II receptor leads to a decrease in airway reactivity in a non-Ag-dependent model. Increased serum levels of IFN-γ can be detected in these animals. In contrast, after injection of OVA …

Epitopes T-LymphocyteNitric Oxide Synthase Type IIImmunoglobulin EMiceAntibody SpecificityCell MovementT-Lymphocyte SubsetsTransforming Growth Factor betaImmunology and AllergyInterferon gammaLungInterleukin-13biologymedicine.diagnostic_testrespiratory systemImmunohistochemistrymedicine.anatomical_structureInterleukin 13Alum Compoundsmedicine.symptomBronchial HyperreactivityBronchoalveolar Lavage Fluidmedicine.drugGenetically modified mousemedicine.medical_specialtyOvalbuminT cellImmunologyCD2 AntigensInflammationMice Inbred StrainsMice TransgenicProtein Serine-Threonine KinasesInterferon-gammaInternal medicineAdministration InhalationmedicineAnimalsHumansAerosolsInflammationbusiness.industryReceptor Transforming Growth Factor-beta Type IITransforming growth factor betaImmunoglobulin ETh1 Cellsrespiratory tract diseasesEndocrinologyBronchoalveolar lavageImmunologybiology.proteinNitric Oxide SynthasebusinessReceptors Transforming Growth Factor betaJournal of immunology (Baltimore, Md. : 1950)
researchProduct