Search results for "experimental"

showing 10 items of 18236 documents

Kinase-independent functions of RIPK1 regulate hepatocyte survival and liver carcinogenesis.

2017

The mechanisms that regulate cell death and inflammation play an important role in liver disease and cancer. Receptor-interacting protein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits kinase-independent prosurvival and proinflammatory functions. Here, we have used genetic mouse models to study the role of RIPK1 in liver homeostasis, injury, and cancer. While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF…

0301 basic medicineProgrammed cell deathLiver tumorCell SurvivalNecroptosisMice TransgenicBiologyChronic liver diseaseProinflammatory cytokine03 medical and health sciencesLiver diseaseMiceLiver Neoplasms ExperimentalmedicineAnimalsDiethylnitrosamineKinase activityTranscription Factor RelAGeneral Medicinemedicine.disease3. Good healthNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticReceptors Tumor Necrosis Factor Type IHepatocyteReceptor-Interacting Protein Serine-Threonine KinasesCancer researchHepatocytesSignal TransductionResearch ArticleThe Journal of clinical investigation
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Cytotoxicity of a naturally occuring spirostanol saponin, progenin III, towards a broad range of cancer cell lines by induction of apoptosis, autopha…

2020

Abstract This study was aimed to investigate the cytotoxic potential of a natural compound, progenin III on a broad range of cancer cell lines, including various sensitive and drug-resistant phenotypes. The cytotoxicity, progenin III-induced autophagic, ferroptotic and necroptotic cell death were evaluated by the resazurin reduction assay (RRA). Spectrophotometric analysis of caspases activity was performed using caspase-Glo assay. Flow cytometry was applied for cell cycle analysis (PI staining), apoptosis (annexin V/PI staining), mitochondrial membrane potential (MMP) (JC-1) and reactive oxygen species (ROS) (H2DCFH-DA). Progenin III and the reference molecule, doxorubicin exerted cytotoxi…

0301 basic medicineProgrammed cell deathNecroptosisMelanoma ExperimentalApoptosisToxicologyFlow cytometry03 medical and health sciences0302 clinical medicineAnnexinCell Line TumorAutophagySpirostansmedicineHumansCytotoxic T cellCytotoxicityCaspaseMembrane Potential MitochondrialCell Deathmedicine.diagnostic_testbiologyPlant ExtractsChemistryCell CycleHep G2 CellsGeneral MedicineSaponinsHCT116 CellsAntineoplastic Agents PhytogenicMolecular biology030104 developmental biologyDoxorubicinDrug Resistance NeoplasmApoptosisCaspases030220 oncology & carcinogenesisNecroptosisbiology.proteinReactive Oxygen SpeciesChemico-Biological Interactions
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Pro- and Antitumorigenic Capacity of Immunoproteasomes in Shaping the Tumor Microenvironment

2021

Abstract Apart from the constitutive proteasome, the immunoproteasome that comprises the three proteolytic subunits LMP2, MECL-1, and LMP7 is expressed in most immune cells. In this study, we describe opposing roles for immunoproteasomes in regulating the tumor microenvironment (TME). During chronic inflammation, immunoproteasomes modulated the expression of protumorigenic cytokines and chemokines and enhanced infiltration of innate immune cells, thus triggering the onset of colitis-associated carcinogenesis (CAC) in wild-type mice. Consequently, immunoproteasome-deficient animals (LMP2/MECL-1/LMP7–null mice) were almost completely resistant to CAC development. In patients with ulcerative c…

0301 basic medicineProteasome Endopeptidase ComplexCancer ResearchChemokineImmunologyMelanoma ExperimentalAntineoplastic AgentsInflammationmedicine.disease_causeArticleMice03 medical and health sciences0302 clinical medicineImmune systemCell Line TumorTumor MicroenvironmentmedicineAnimalsHumansMice KnockoutTumor microenvironmentInnate immune systembiologyChemistryMelanomaHistocompatibility Antigens Class IColitismedicine.diseaseMice Inbred C57BLCysteine Endopeptidases030104 developmental biology030220 oncology & carcinogenesisCancer researchbiology.proteinCytokinesFemalemedicine.symptomCarcinogenesisCD8T-Lymphocytes CytotoxicCancer Immunology Research
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Lack of NFATc1 SUMOylation prevents autoimmunity and alloreactivity

2020

A novel transgenic mouse, in which the transcription factor NFATc1 bears lysine-to-arginine mutations that prevent modification by SUMO, develops normally and is healthy. However, SUMO-insensitive NFATc1 transmits strong tolerogenic signals, thus preventing autoimmune and alloimmune T cell responses.

0301 basic medicineProtein sumoylationEncephalomyelitis Autoimmune ExperimentalT cellStem Cells & RegenerationImmunologySUMO proteinAutoimmunityBiologyenvironment and public healthT-Lymphocytes RegulatoryArticleMinor Histocompatibility AntigensMice03 medical and health sciences0302 clinical medicineImmune systemNeuroinflammationAldesleukinSTAT5 Transcription FactormedicineAnimalsImmunology and AllergyTranscription factorMice Knockoutintegumentary systemNFATC Transcription FactorsExperimental autoimmune encephalomyelitisSumoylationNFATmedicine.diseaseCell biologyenzymes and coenzymes (carbohydrates)030104 developmental biologymedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisCytokinesPositive Regulatory Domain I-Binding Factor 1Journal of Experimental Medicine
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The Small Heat Shock Protein α-Crystallin B Shows Neuroprotective Properties in a Glaucoma Animal Model

2017

Glaucoma is a neurodegenerative disease that leads to irreversible retinal ganglion cell (RGC) loss and is one of the main causes of blindness worldwide. The pathogenesis of glaucoma remains unclear, and novel approaches for neuroprotective treatments are urgently needed. Previous studies have revealed significant down-regulation of α-crystallin B as an initial reaction to elevated intraocular pressure (IOP), followed by a clear but delayed up-regulation, suggesting that this small heat-shock protein plays a pathophysiological role in the disease. This study analyzed the neuroprotective effect of α-crystallin B in an experimental animal model of glaucoma. Significant IOP elevation induced b…

0301 basic medicineProteomicsRetinal Ganglion Cellsgenetic structuresNerve fiber layerGlaucomaCell CountMass Spectrometrylcsh:ChemistryPathogenesischemistry.chemical_compound0302 clinical medicineexperimental glaucoma; α-crystallin B; neuroprotection; proteomicsProtein Interaction Mapslcsh:QH301-705.5Spectroscopyα-crystallin BGeneral MedicineComputer Science ApplicationsUp-Regulationmedicine.anatomical_structureNeuroprotective AgentsRetinal ganglion cellneuroprotectionRetinal Neuronsmedicine.medical_specialtyDown-RegulationBiologyNeuroprotectionCatalysisArticleInorganic Chemistry03 medical and health sciencesCrystallinOphthalmologyHeat shock proteinmedicineElectroretinographyAnimalsPhysical and Theoretical ChemistryMolecular BiologyIntraocular Pressureexperimental glaucomaOrganic Chemistryalpha-Crystallin B ChainRetinalGlaucomamedicine.diseaseeye diseasesDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistry030221 ophthalmology & optometrysense organsInternational Journal of Molecular Sciences; Volume 18; Issue 11; Pages: 2418
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Linezolid and atorvastatin impact on pneumonia caused by Staphyloccocus aureus in rabbits with or without mechanical ventilation

2017

International audience; Pneumonia may involve methicillin-resistant Staphylococcus aureus (MRSA), with elevated rates of antibiotics failure. The present study aimed to assess the effect of statins given prior to pneumonia development. Spontaneously breathing (SB) or mechanically ventilated (MV) rabbits with pneumonia received atorvastatin alone, linezolid (LNZ) alone, or a combination of both (n = 5 in each group). Spontaneously breathing and MV untreated infected animals (n = 11 in each group), as well as uninfected animals (n = 5 in each group) were used as controls. Microbiological features and inflammation were evaluated. Data are presented as medians (interquartile range). Linezolid a…

0301 basic medicinePulmonologyPhysiologymedicine.medical_treatmentAtorvastatinStaphylococcuslcsh:MedicineInduced Lung Injurychemistry.chemical_compound0302 clinical medicineImmune PhysiologyMedicine and Health SciencesAtorvastatinlcsh:ScienceImmune ResponseLungPathology and laboratory medicineMammalsInnate Immune SystemMultidisciplinaryRespirationDrugsEukaryotaAnimal ModelsMedical microbiology3. Good healthBody FluidsUp-Regulationmedicine.anatomical_structureBloodExperimental Organism SystemsBreathingAnesthesiaVertebratesLeporidsCytokinesMethicillin-resistant Staphylococcus aureusRabbitsPathogensAnatomyIn-Vivomedicine.drugResearch Article[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT]Staphylococcus aureusStatinmedicine.drug_class030106 microbiologyImmunologyOutcomesResearch and Analysis MethodsMicrobiologySepsis03 medical and health sciencesSigns and SymptomsDiagnostic MedicineSepsismedicinePneumonia BacterialAnimalsTidal-VolumeMortality[ SDV.OT ] Life Sciences [q-bio]/Other [q-bio.OT]Mechanical ventilationPharmacologyInflammationLungBacteriabusiness.industrylcsh:ROrganismsLinezolidStatinsBiology and Life Sciences030208 emergency & critical care medicinePneumoniaMolecular Developmentmedicine.diseaseRespiration ArtificialToll-Like Receptor 2Microbial pathogensPneumoniachemistryBacteremiaImmune SystemLinezolidAmnioteslcsh:QBacterial pathogensbusinessPhysiological ProcessesDevelopmental BiologyModel
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Transcription factor NRF2 as a therapeutic target for chronic diseases: a systems medicine approach

2018

Systems medicine has a mechanism-based rather than a symptom- or organ-based approach to disease and identifies therapeutic targets in a nonhypothesis-driven manner. In this work, we apply this to transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2) by cross-validating its position in a protein-protein interaction network (the NRF2 interactome) functionally linked to cytoprotection in low-grade stress, chronic inflammation, metabolic alterations, and reactive oxygen species formation. Multiscale network analysis of these molecular profiles suggests alterations of NRF2 expression and activity as a common mechanism in a subnetwork of diseases (the NRF2 diseasome). This netw…

0301 basic medicineRMSystems AnalysisNF-E2-Related Factor 2MedicinaNF-KAPPA-BAnti-Inflammatory AgentsTYPE-2 DIABETES-MELLITUSGENE PROMOTER POLYMORPHISMDiseaseComputational biologyInteractomeenvironment and public healthGLYCOGEN-SYNTHASE KINASETUMOR-SUPPRESSOR PTENNRF203 medical and health sciencesDrug DiscoveryAnimalsHumansTherapeutic targetsMedicineMolecular Targeted TherapyBardoxolone methylPLACEBO-CONTROLLED PHASE-3PharmacologyMechanism (biology)Drug discoverybusiness.industryDrug RepositioningRChronic inflammationrespiratory systemHEME OXYGENASE 1PROTEIN-PROTEIN INTERACTION3. Good healthSystems medicineDrug repositioning030104 developmental biologyDrug developmentEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISChronic DiseaseSystems medicineMolecular MedicineFUMARIC-ACID ESTERSbusiness
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The actin remodeling protein cofilin is crucial for thymic αβ but not γδ T-cell development

2018

Cofilin is an essential actin remodeling protein promoting depolymerization and severing of actin filaments. To address the relevance of cofilin for the development and function of T cells in vivo, we generated knock-in mice in which T-cell–specific nonfunctional (nf) cofilin was expressed instead of wild-type (WT) cofilin. Nf cofilin mice lacked peripheral αβ T cells and showed a severe thymus atrophy. This was caused by an early developmental arrest of thymocytes at the double negative (DN) stage. Importantly, even though DN thymocytes expressed the TCRβ chain intracellularly, they completely lacked TCRβ surface expression. In contrast, nf cofilin mice possessed normal numbers of γδ T cel…

0301 basic medicineReceptors Antigen T-Cell alpha-betaT-LymphocytesJurkat cellsenvironment and public healthImmune ReceptorsBiochemistryWhite Blood CellsJurkat CellsMice0302 clinical medicineContractile ProteinsSpectrum Analysis TechniquesShort ReportsAnimal CellsCell MovementT-Lymphocyte SubsetsMedicine and Health SciencesGene Knock-In TechniquesBiology (General)Post-Translational ModificationPhosphorylationThymocytesImmune System ProteinsT CellsGeneral NeuroscienceStem CellsReceptors Antigen T-Cell gamma-deltaTransfectionAnimal ModelsCofilinFlow CytometryCell biologyThymusmedicine.anatomical_structureExperimental Organism SystemsActin Depolymerizing FactorsSpectrophotometry030220 oncology & carcinogenesisPhosphorylationCytophotometryCellular TypesGeneral Agricultural and Biological SciencesSignal TransductionHematopoietic Progenitor CellsProlineQH301-705.5T cellImmune CellsImmunologyDouble negativeMouse Modelsmacromolecular substancesThymus GlandBiologyResearch and Analysis MethodsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesModel OrganismsmedicineAnimalsHumansActinBlood CellsGeneral Immunology and MicrobiologyActin remodelingBiology and Life SciencesProteinsCell BiologyActinsT Cell ReceptorsCytoskeletal Proteins030104 developmental biologyImmune SystemMutationPLoS Biology
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A T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis.

2017

Multiple sclerosis (MS) is a human neurodegenerative disease characterized by the invasion of autoreactive T cells from the periphery into the CNS. Application of pan-histone deacetylase inhibitors (HDACi) ameliorates experimental autoimmune encephalomyelitis (EAE), an animal model for MS, suggesting that HDACi might be a potential therapeutic strategy for MS. However, the function of individual HDAC members in the pathogenesis of EAE is not known. In this study we report that mice with a T cell-specific deletion of HDAC1 (using the Cd4-Cre deleter strain; HDAC1-cKO) were completely resistant to EAE despite the ability of HDAC1cKO CD4+ T cells to differentiate into Th17 cells. RNA sequencin…

0301 basic medicineReceptors CCR6Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisReceptors CCR4T cellImmunologyCCR4Histone Deacetylase 1C-C chemokine receptor type 6Biologymedicine.disease_causeAutoimmunity03 medical and health sciencesChemokine receptorMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsHumansCells CulturedMice KnockoutChimeraMultiple sclerosisExperimental autoimmune encephalomyelitisGene targetingmedicine.diseaseMolecular biologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureSTAT1 Transcription FactorCancer researchTh17 Cells030215 immunologyJournal of autoimmunity
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Generation of an inducible RPE-specific Cre transgenic-mouse line.

2018

The retinal pigment epithelium (RPE) is an epithelial monolayer in the back of the vertebrate eye. RPE dysfunction is associated with retinal degeneration and blindness. In order to fully understand how dysregulation affects visual function, RPE-specific gene knockouts are indispensable. Since the currently available RPE-specific Cre recombinases show lack of specificity or poor recombination, we sought to generate an alternative. We generated a tamoxifen-inducible RPE-specific Cre transgenic mouse line under transcriptional control of an RPE-specific Tyrosinase enhancer. We characterized the Cre-mediated recombinant expression by crossing our RPE-Tyrosinase-CreErT2 mouse line with the tdTo…

0301 basic medicineRetinal degenerationMaleEmbryologylcsh:MedicineGene ExpressionRetinal Pigment EpitheliumBiochemistry0302 clinical medicineRecombinaseMedicine and Health Scienceslcsh:ScienceStainingMultidisciplinaryMonophenol MonooxygenaseAnimal ModelsSpecimen preparation and treatmentCell biologyEnzymesmedicine.anatomical_structureExperimental Organism SystemsModels AnimalFemaleAnatomyResearch ArticleGenetically modified mouseImaging TechniquesTransgeneOcular AnatomyMice TransgenicMouse ModelsBiologyResearch and Analysis MethodsRetinaRecombinases03 medical and health sciencesModel OrganismsOcular SystemFluorescence ImagingmedicineGeneticsAnimalsEnhancerGene knockoutRetinaRetinal pigment epitheliumIntegraseslcsh:REmbryosDAPI stainingBiology and Life SciencesProteinsmedicine.diseaseeye diseasesMice Inbred C57BLLuminescent Proteins030104 developmental biologyNuclear stainingEnzymologyAnimal StudiesEyeslcsh:Qsense organsHead030217 neurology & neurosurgeryDevelopmental BiologyPloS one
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