Search results for "Disease Model"

showing 10 items of 1116 documents

Imatinib spares cKit-expressing prostate neuroendocrine tumors, whereas kills seminal vesicle epithelial-stromal tumors by targeting PDGFR-β

2017

Abstract Prostate cancer is a leading cause of cancer-related death in males worldwide. Indeed, advanced and metastatic disease characterized by androgen resistance and often associated with neuroendocrine (NE) differentiation remains incurable. Using the spontaneous prostate cancer TRAMP model, we have shown that mast cells (MCs) support in vivo the growth of prostate adenocarcinoma, whereas their genetic or pharmacologic targeting favors prostate NE cancer arousal. Aiming at simultaneously targeting prostate NE tumor cells and MCs, both expressing the cKit tyrosine kinase receptor, we have tested the therapeutic effect of imatinib in TRAMP mice. Imatinib-treated TRAMP mice experience a pa…

0301 basic medicineMaleCancer ResearchReceptor tyrosine kinaseAntineoplastic AgentProstate cancerMice0302 clinical medicineProstatebiologySeminal VesiclesImmunohistochemistryGene Expression Regulation NeoplasticNeuroendocrine TumorsProto-Oncogene Proteins c-kitmedicine.anatomical_structureOncology030220 oncology & carcinogenesisImatinib MesylateFemaleNeuroendocrine Tumormedicine.drugTrampHumanSignal TransductionPCA3medicine.medical_specialtyStromal cellXenograft Model Antitumor AssayProtein Kinase InhibitorAntineoplastic AgentsMice TransgenicReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesInternal medicineSeminal VesiclemedicineAnimalsHumansProtein Kinase InhibitorsAnimalProstatic NeoplasmsImatinibBiomarkermedicine.diseaseXenograft Model Antitumor AssaysDisease Models Animal030104 developmental biologyEndocrinologyImatinib mesylateProstatic Neoplasmbiology.proteinCancer researchBiomarkers
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Rhythmic Regulation of Photoreceptor and RPE Genes Important for Vision and Genetically Associated With Severe Retinal Diseases.

2018

Purpose The aim of the present study was to identify candidate genes for mediating daily adjustment of vision. Methods Genes important for vision and genetically associated with severe retinal diseases were tested for 24-hour rhythms in transcript levels in neuronal retina, microdissected photoreceptors, photoreceptor-related pinealocytes, and retinal pigment epithelium-choroid (RPE-choroid) complex by using quantitative PCR. Results Photoreceptors of wildtype mice display circadian clock-dependent regulation of visual arrestins (Arr1, Arr4) and the visual cycle gene Rdh12, whereas cells of the RPE-choroid exhibit light-dependent regulation of the visual cycle key genes Lrat, Rpe65, and Rdh…

0301 basic medicineMaleCandidate genegenetic structuresArrestinsRetinal Pigment EpitheliumBiologyRetinaPinealocyte570 Life sciencesvisual cyclevisual arrestinRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compoundMiceRetinal DiseasesmedicineElectroretinographyAnimalsCircadian rhythmVision OcularRetinaDiabetic Retinopathymedicine.diagnostic_testRetinal DehydrogenaseRetinalcircadian regulationeye diseasesCell biologyCircadian RhythmRatsMice Inbred C57BLAlcohol OxidoreductasesDisease Models Animal030104 developmental biologymedicine.anatomical_structureRPE65chemistryGene Expression RegulationRetinal Cone Photoreceptor CellsFemalesense organsElectroretinographyVisual phototransduction570 BiowissenschaftenInvestigative ophthalmologyvisual science
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Intranasal Administration of Extracellular Vesicles Derived from Human Teeth Stem Cells Improves Motor Symptoms and Normalizes Tyrosine Hydroxylase E…

2018

Abstract Parkinson's disease (PD) is the second most common neurodegenerative disorder affecting millions of people worldwide. At present, there is no effective cure for PD; treatments are symptomatic and do not halt progression of neurodegeneration. Extracellular vesicles (EVs) can cross the blood–brain barrier and represent promising alternative to the classical treatment strategies. In the present study, we examined therapeutic effects of intranasal administration of EVs derived from human exfoliated deciduous teeth stem cells (SHEDs) on unilateral 6-hydroxydopamine (6-OHDA) medial forebrain bundle (MFB) rat model of PD. CatWalk gait tests revealed that EVs effectively suppressed 6-OHDA-…

0301 basic medicineMaleCell signalingParkinson's diseaseParkinson's diseaseStriatumPharmacology0302 clinical medicineMedicineMedial forebrain bundleAdult stem cellsStem CellsNeurodegenerationParkinson DiseaseGeneral MedicineAnimal modelsSubstantia NigraDifferentiationmedicine.symptom:MEDICINE::Physiology and pharmacology::Pharmacological research [Research Subject Categories]Tyrosine 3-MonooxygenaseCellular therapySubstantia nigraLesion03 medical and health sciencesExtracellular VesiclesMicroscopy Electron TransmissionTissue Engineering and Regenerative MedicineAnimalsHumansRats WistarOxidopamineAdministration IntranasalAgedHydroxydopamineTyrosine hydroxylasebusiness.industryCell Biologymedicine.diseaseCorpus StriatumRatsDisease Models Animal030104 developmental biologynervous systemMesenchymal stem cellsbusinessTooth030217 neurology & neurosurgeryDevelopmental BiologyStem cells translational medicine
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General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation.

2016

Relapsing-remitting multiple sclerosis (MS)(2) is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).(3) The molecular mechanisms responsible for directing Tregs into the inflamed CNS tissue, however, are incompletely understood. In an MS mouse model we show that the stress kinase general control non-derepressible 2 (GCN2),(4) expressed in T cells, contributes to the resolution of autoimmune neuroinflammation. Failure to recover from acute inflammation was associated with reduced frequencies of CNS-infiltrating Tregs. GCN2 deficient Tregs displayed impaired migration to a…

0301 basic medicineMaleChemokineEncephalomyelitis Autoimmune ExperimentalTime FactorsT cellImmunologyInflammationSpontaneous remissionMice TransgenicCCL2Protein Serine-Threonine KinasesT-Lymphocytes RegulatoryStatistics Nonparametric03 medical and health sciencesMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsAnnexin A5NeuroinflammationbiologyKinaseMultiple sclerosisBrainEndothelial Cellsmedicine.diseaseFlow CytometryPeptide FragmentsMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesImmunologybiology.proteinDisease ProgressionCytokinesFemaleMyelin-Oligodendrocyte GlycoproteinNeurology (clinical)medicine.symptom030215 immunologyJournal of neuroimmunology
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Alzheimer's disease in the gut : major changes in the gut of 5xFAD model mice with ApoA1 as potential key player

2019

Alzheimer's disease (AD) affects around 33 million people worldwide, which makes it the most prominent form of dementia. The main focus of AD research has been on the central nervous system (CNS) for long, but in recent years, the gut gained more attention. The intestinal tract is innervated by the enteric nervous system (ENS), built of numerous different types of neurons showing great similarity to neurons of the CNS. It already has been demonstrated that the amyloid precursor protein, which plays a major role in AD pathology, is also expressed in these cells. We analyzed gut tissue of AD model mice (5xFAD) and the respective wild-type littermates at different pathological stages: pre-path…

0301 basic medicineMaleColonCentral nervous system610 MedizinMice TransgenicDiseaseBiochemistryEnteric Nervous System03 medical and health sciencesMice0302 clinical medicineAlzheimer Disease610 Medical sciencesGeneticsmedicineAmyloid precursor proteinDementiaAnimalsViability assayMolecular BiologyPathologicalbiologyApolipoprotein A-Imedicine.diseaseDisease Models Animal030104 developmental biologymedicine.anatomical_structureImmunologybiology.proteinEnteric nervous systemFOXA2030217 neurology & neurosurgeryBiotechnology
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Targeting aurora kinase B alleviates spinal microgliosis and neuropathic pain in a rat model of peripheral nerve injury.

2019

Peripheral nerve injury elicits spinal microgliosis, contributing to neuropathic pain. The aurora kinases A (AURKA), B (AURKB), and C (AURKC) are potential therapeutic targets in proliferating cells. However, their role has not been clarified in microglia. The aim of this study was to examine the regulation of aurora kinases and their roles and druggability in spinal microgliosis and neuropathic pain. Sprague-Dawley rats received chronic constriction injury (CCI). Gene expression of aurora kinases A-C was evaluated by quantitative RT-PCR and western blot, respectively, in spinal cords at 1, 3, 7, and 14 days after CCI. AURKB gene and protein expression was up-regulated concomitantly with th…

0301 basic medicineMaleDown-RegulationGene ExpressionMicrogliosisBiochemistryRats Sprague-Dawley03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinePeripheral Nerve InjuriesMedicineAnimalsAurora Kinase BAURKB GeneEnzyme InhibitorsGene knockdownMicrogliabusiness.industryKinaseSpinal cordRatsDisease Models Animal030104 developmental biologymedicine.anatomical_structureSpinal CordGene Knockdown TechniquesPeripheral nerve injuryNeuropathic painCancer researchNeuralgiaMicrogliabusiness030217 neurology & neurosurgeryJournal of neurochemistryReferences
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Gut Microbiota Restricts NETosis in Acute Mesenteric Ischemia-Reperfusion Injury.

2020

Objective: Recruitment of neutrophils and formation of neutrophil extracellular traps (NETs) contribute to lethality in acute mesenteric infarction. To study the impact of the gut microbiota in acute mesenteric infarction, we used gnotobiotic mouse models to investigate whether gut commensals prime the reactivity of neutrophils towards formation of neutrophil extracellular traps (NETosis). Approach and Results: We applied a mesenteric ischemia-reperfusion (I/R) injury model to germ-free (GF) and colonized C57BL/6J mice. By intravital imaging, we quantified leukocyte adherence and NET formation in I/R-injured mesenteric venules. Colonization with gut microbiota or monocolonization with Esch…

0301 basic medicineMaleExtracellular TrapsMesenteric infarctionLipopolysaccharideNeutrophilsGut floraExtracellular Traps03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAcute mesenteric ischemiaVenulesmedicineCell AdhesionEscherichia coliLeukocytesAnimalsGerm-Free LifeLeukocyte RollingMesenteryCells CulturedMice Knockoutbiologybusiness.industryNeutrophil extracellular trapsbiology.organism_classificationmedicine.diseaseGastrointestinal MicrobiomeMice Inbred C57BLToll-Like Receptor 4Disease Models Animal030104 developmental biologychemistryNeutrophil Infiltration030220 oncology & carcinogenesisMesenteric IschemiaReperfusion InjuryImmunologyHost-Pathogen InteractionsFemaleCardiology and Cardiovascular MedicinebusinessReperfusion injuryBacillus subtilisSignal TransductionArteriosclerosis, thrombosis, and vascular biology
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Interferon-γ-Driven iNOS: A Molecular Pathway to Terminal Shock in Arenavirus Hemorrhagic Fever

2017

Arenaviruses such as Lassa virus (LASV) cause hemorrhagic fever. Terminal shock is associated with a systemic cytokine storm, but the mechanisms are ill defined. Here we used HLA-A2-expressing mice infected with a monkey-pathogenic strain of lymphocytic choriomeningitis virus (LCMV-WE), a close relative of LASV, to investigate the pathophysiology of arenavirus hemorrhagic fever (AHF). AHF manifested as pleural effusions, edematous skin swelling, and serum albumin loss, culminating in hypovolemic shock. A characteristic cytokine storm included numerous pro-inflammatory cytokines and nitric oxide (NO) metabolites. Edema formation and terminal shock were abrogated in mice lacking inducible nit…

0301 basic medicineMaleHemorrhagic Fevers ViralNitric Oxide Synthase Type IIBiologyLymphocytic Choriomeningitisddc:616.07Lymphocytic choriomeningitismedicine.disease_causeNitric OxideMicrobiologyViral hemorrhagic fever03 medical and health sciencesInterferon-gammaMice0302 clinical medicineVirologymedicineAnimalsHumansLymphocytic choriomeningitis virusLassa feverArenavirusddc:617medicine.diseasebiology.organism_classification3. Good healthNitric oxide synthaseMice Inbred C57BLDisease Models Animal030104 developmental biologyLassa virus030220 oncology & carcinogenesisShock (circulatory)Immunologybiology.proteinParasitologyFemalemedicine.symptomCytokine storm
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Multicomponent Training Prevents Memory Deficit Related to Amyloid-β Protein-Induced Neurotoxicity.

2021

Background: Alzheimer’s disease (AD) is characterized by the accumulation of the amyloid-β peptide in the brain, leading to early oxidative stress and neurotoxicity. It has been suggested that physical exercise could be beneficial in preventing AD, but studies with multicomponent training are scanty. Objective: Verify the effects of multicomponent exercise training to prevent deficits in recognition memory related to Aβ neurotoxicity. Methods: We subjected Wistar rats to multicomponent training (including aerobic and anaerobic physical exercise and cognitive exercise) and then infused amyloid-β peptide into their hippocampus. Results: We show that long-term multicomponent training prevents …

0301 basic medicineMaleHippocampusPhysical exercisePharmacologyHippocampal formationmedicine.disease_causeHippocampusLipid peroxidationStereotaxic Techniques03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysical Conditioning AnimalMedicineAnimalsRats WistarRecognition memoryMemory DisordersAmyloid beta-Peptidesbusiness.industryGeneral NeuroscienceNeurotoxicityBrainGeneral Medicinemedicine.diseaseRatsPsychiatry and Mental healthClinical PsychologyDisease Models AnimalOxidative Stress030104 developmental biologychemistryNeurotoxicity SyndromesLipid PeroxidationGeriatrics and GerontologybusinessAnaerobic exercise030217 neurology & neurosurgeryOxidative stressJournal of Alzheimer's disease : JAD
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Plasmacytoid dendritic cells promote systemic sclerosis with a key role for TLR8

2018

Systemic sclerosis (SSc) is a multisystem life-threatening fibrosing disorder that lacks effective treatment. The link between the inflammation observed in organs such as the skin and profibrotic mechanisms is not well understood. The plasmacytoid dendritic cell (pDC) is a key cell type mediating Toll-like receptor (TLR)-induced inflammation in autoimmune disease patients, including lupus and skin diseases with interface dermatitis. However, the role of pDCs in fibrosis is less clear. We show that pDCs infiltrate the skin of SSc patients and are chronically activated, leading to secretion of interferon-α (IFN-α) and CXCL4, which are both hallmarks of the disease. We demonstrate that the s…

0301 basic medicineMaleInflammationPlasmacytoid dendritic cellPlatelet Factor 4SclerodermaArticlePathogenesis03 medical and health sciencesBleomycinMice0302 clinical medicineFibrosismedicineAnimalsHumansSkin030203 arthritis & rheumatologyAutoimmune diseaseSystemic lupus erythematosusScleroderma Systemicintegumentary systembusiness.industryMedicine (all)Interferon-alphahemic and immune systemsGeneral MedicineTLR7Dendritic CellsMiddle Agedmedicine.diseaseFibrosisDisease Models Animal030104 developmental biologyToll-Like Receptor 7Toll-Like Receptor 8ImmunologyFemalemedicine.symptombusinessSignal Transduction
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