Search results for "C57BL"

showing 10 items of 1292 documents

Induction of Chromosome Instability by Activation of Yes-Associated Protein and Forkhead Box M1 in Liver Cancer

2016

Background & Aims Many different types of cancer cells have chromosome instability. The hippo pathway leads to phosphorylation of the transcriptional activator yes-associated protein 1 (YAP1, YAP), which regulates proliferation and has been associated with the development of liver cancer. We investigated the effects of hippo signaling via YAP on chromosome stability and hepatocarcinogenesis in humans and mice. Methods We analyzed transcriptome data from 242 patients with hepatocellular carcinoma (HCC) to search for gene signatures associated with chromosomal instability (CIN); we investigated associations with overall survival time and cancer recurrence using Kaplan–Meier curves. We analyze…

0301 basic medicineTime FactorsMuscle ProteinsKaplan-Meier Estimatemedicine.disease_causeChromosome instabilityYAP1Liver NeoplasmsGastroenterologyTEA Domain Transcription FactorsHep G2 CellsPrognosisDNA-Binding ProteinsGene Expression Regulation NeoplasticPhenotypeHippo signalingRNA InterferenceSignal TransductionCarcinoma HepatocellularPorphyrinsAntineoplastic AgentsMice TransgenicBiologyTransfection03 medical and health sciencesChromosomal InstabilitymedicineAnimalsHumansGene silencingGenetic Predisposition to DiseaseAdaptor Proteins Signal TransducingHippo signaling pathwayHepatologyGene Expression ProfilingForkhead Box Protein M1VerteporfinYAP-Signaling ProteinsHCCSPhosphoproteinsThiostreptonMolecular biologyMice Inbred C57BLDisease Models Animal030104 developmental biologyTissue Array AnalysisFOXM1Cancer researchTranscriptomeCarcinogenesisTranscription FactorsGastroenterology
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Alternative Splice Forms of CYLD Mediate Ubiquitination of SMAD7 to Prevent TGFB Signaling and Promote Colitis

2018

Background & Aims The CYLD lysine 63 deubiquitinase gene (CYLD) encodes tumor suppressor protein that is mutated in familial cylindromatosus, and variants have been associated with Crohn disease (CD). Splice forms of CYLD that lack exons 7 and 8 regulate transcription factors and functions of immune cells. We examined the expression of splice forms of CYLD in colon tissues from patients with CD and their effects in mice. Methods We performed immunohistochemical analyses of colon tissues from patients with untreated CD and patients without inflammatory bowel diseases (controls). We obtained mice that expressed splice forms of CYLD (sCYLD mice) without or with SMAD7 (sCYLD/SMAD7 mice) from tr…

0301 basic medicineTranscription FactorBiopsyInbred C57BLTransgenicImmune RegulationSettore MED/12MiceRandom Allocation0302 clinical medicineCrohn DiseaseReference ValuesNeedleIntestinal Mucosaintegumentary systemChemistryBiopsy NeedleGastroenterologyT helper cellFlow CytometryPost-translational ModificationImmunohistochemistryDeubiquitinating Enzyme CYLDCysteine Endopeptidasesmedicine.anatomical_structure030211 gastroenterology & hepatologyTumor necrosis factor alphaSignal TransductionGenetically modified mouseRegulatory T cellTransgeneMice TransgenicSmad7 ProteinTransforming Growth Factor beta103 medical and health sciencesImmune systemmedicineAnimalsHumansCytokine SignalingHepatologyAnimalHEK 293 cellsUbiquitinationMolecular biologyMice Inbred C57BLDisease Models Animal030104 developmental biologyDisease ModelsCytokine Signaling; Immune Regulation; Post-translational Modification; Transcription Factor; Biopsy Needle; Crohn Disease; Cysteine Endopeptidases; Deubiquitinating Enzyme CYLD; Disease Models Animal; Flow Cytometry; Immunohistochemistry; Intestinal Mucosa; Mice Inbred C57BL; Mice Transgenic; Random Allocation; Reference Values; Signal Transduction; Smad7 Protein; Transforming Growth Factor beta1; UbiquitinationTransforming growth factorGastroenterology
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Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation

2015

Unwinding DNA and unleasing inflammation Fighting infections often comes with collateral damage, which sometimes can be deadly. For instance, in septic shock, the overwhelming release of inflammatory mediators drives multi-organ failure. Rialdi et al. now report a potential new therapeutic target for controlling excessive inflammation: the DNA unwinding enzyme topoisomerase I (Top1) (see the Perspective by Pope and Medzhitov). Upon infection, Top1 specifically localizes to the promoters of pathogen-induced genes and promotes their transcription by helping to recruit RNA polymerase II. Pharmacological inhibition of Top1 in a therapeutic setting increased survival in several mouse models of s…

0301 basic medicineTranscription GeneticType IInbred C57BLmedicine.disease_causeSendai virusMicePiperidinesTranscription (biology)Influenza A virusInnate2.1 Biological and endogenous factorsPositive Transcriptional Elongation Factor BAetiologyMultidisciplinaryAzepinesStaphylococcal InfectionsEbolavirusInfectious DiseasesDNA Topoisomerases Type IInfluenza A virusEbolaHost-Pathogen InteractionsPneumonia & InfluenzaRNA Polymerase IImedicine.symptomInfectionTranscriptionStaphylococcus aureusGeneral Science & TechnologyInflammationBiologyVaccine Related03 medical and health sciencesImmune systemGeneticImmunityBiodefenseGeneticsmedicineAnimalsHumansGeneFlavonoidsInflammationInnate immune systemPreventionHEK 293 cellsImmunityInterferon-betaHemorrhagic Fever EbolaTriazolesImmunity InnateMice Inbred C57BLEmerging Infectious DiseasesGood Health and Well BeingHEK293 Cells030104 developmental biologyGene Expression RegulationImmunologyCancer researchHemorrhagic FeverCamptothecinTopoisomerase I InhibitorsTopotecanDNA TopoisomerasesScience
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Negative transfer effects between reference memory and working memory training in the water maze in C57BL/6 mice

2017

The water maze is one of the most widely employed spatial learning paradigms in the cognitive profiling of genetically modified mice. Oftentimes, tests of reference memory (RM) and working memory (WM) in the water maze are sequentially evaluated in the same animals. However, critical difference in the rules governing efficient escape from the water between WM and RM tests is expected to promote the adoption of incompatible mnemonic or navigational strategies. Hence, performance in a given test is likely poorer if it follows the other test instead of being conducted first. Yet, the presence of such negative transfer effects (or proactive interference) between WM and RM training in the water …

0301 basic medicineWorking memory trainingMaleCIENCIAS MÉDICAS Y DE LA SALUDTransfer PsychologyInterference theoryWATER MAZEInmunologíaNegative transferSpatial BehaviorMnemonicWater mazeMOUSEDevelopmental psychology03 medical and health sciencesBehavioral NeuroscienceTRANSFER EFFECT0302 clinical medicineAnimalsAttentionMaze LearningBehavior AnimalWorking memoryCognitionMice Inbred C57BLMedicina Básica030104 developmental biologyMemory Short-TermSPATIAL LEARNINGReference memoryPsychology030217 neurology & neurosurgeryCognitive psychology
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The HSP90 inhibitor, 17AAG, protects the intestinal stem cell niche and inhibits graft versus host disease development.

2016

IF 7.932; International audience; Graft versus host disease (GvHD), which is the primary complication of allogeneic bone marrow transplantation, can alter the intestinal barrier targeted by activated donor T-cells. Chemical inhibition of the stress protein HSP90 was demonstrated in vitro to inhibit T-cell activation and to modulate endoplasmic reticulum (ER) stress to which intestinal cells are highly susceptible. Since the HSP90 inhibitor 17-allylamino-demethoxygeldanamycin (17AAG) is developed in clinics, we explored here its ability to control intestinal acute GvHD in vivo in two mouse GvHD models (C57BL/6 -> BALB/c and FVB/N -> Lgr5-eGFP), ex vivo in intestine organoids and in vitro in …

0301 basic medicineX-Box Binding Protein 1Cancer ResearchLactams MacrocyclicRNA SplicingT-CellsGraft vs Host Disease[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology[ SDV.CAN ] Life Sciences [q-bio]/CancerHsp90 inhibitor03 medical and health sciencesMiceSensitivityInflammatory-Bowel-diseaseGeneticsmedicineBenzoquinonesAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyNeural progenitor cellsHSP90 Heat-Shock ProteinsIntestinal MucosaStem Cell Niche[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human genetics[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular BiologyLeukemia[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyBone-Marrow-TransplantationMoleculesmedicine.diseaseStem cell niche3. Good healthIre1-AlphaIntestinesMice Inbred C57BL030104 developmental biologyGraft-versus-host diseaseEr Stress[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsCytoprotectionImmunologyMultiple-MyelomaFemaleOncogene
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Junctional adhesion molecules JAM-B and JAM-C promote autoimmune-mediated liver fibrosis in mice

2018

Fibrosis remains a serious health concern in patients with chronic liver disease. We recently reported that chemically induced chronic murine liver injury triggers increased expression of junctional adhesion molecules (JAMs) JAM-B and JAM-C by endothelial cells and de novo synthesis of JAM-C by hepatic stellate cells (HSCs). Here, we demonstrate that biopsies of patients suffering from primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) or autoimmune hepatitis (AIH) display elevated levels of JAM-C on portal fibroblasts (PFs), HSCs, endothelial cells and cholangiocytes, whereas smooth muscle cells expressed JAM-C constitutively. Therefore, localization and function of JA…

0301 basic medicine[SDV]Life Sciences [q-bio]Cholangitis SclerosingMyocytes Smooth MuscleeducationImmunologyImmunoglobulinsAutoimmune hepatitisVascular RemodelingChronic liver diseaseMural cellPrimary sclerosing cholangitisFatty Acids MonounsaturatedMice03 medical and health sciencesFibrosisCell AdhesionmedicineAnimalsHumansImmunology and AllergyMyofibroblastsCells CulturedInflammationMice KnockoutFibrous capsule of GlissonLiver Cirrhosis Biliarybusiness.industryfungiEndothelial Cellsmedicine.diseaseFibrosishumanities3. Good healthMice Inbred C57BLDisease Models AnimalHepatitis Autoimmune030104 developmental biologyLiverVasoconstrictioncardiovascular systemCancer researchHepatic stellate cellFemaleHepatic fibrosisbusinessCell Adhesion MoleculesJournal of Autoimmunity
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Impaired Kupffer Cell Self-Renewal Alters the Liver Response to Lipid Overload during Non-alcoholic Steatohepatitis

2020

International audience; Kupffer cells (KCs) are liver-resident macrophages that self-renew by proliferation in the adult independently from monocytes. However, how they are maintained during non-alcoholic steatohepatitis (NASH) remains ill defined. We found that a fraction of KCs derived from Ly-6C+ monocytes during NASH, underlying impaired KC self-renewal. Monocyte-derived KCs (MoKCs) gradually seeded the KC pool as disease progressed in a response to embryo-derived KC (EmKC) death. Those MoKCs were partly immature and exhibited a pro-inflammatory status compared to EmKCs. Yet, they engrafted the KC pool for the long term as they remained following disease regression while acquiring matur…

0301 basic medicine[SDV]Life Sciences [q-bio]OntogenyMESH: Cell Self RenewalSelf renewalMESH: MonocytesMESH: Mice KnockoutMice0302 clinical medicineNon-alcoholic Fatty Liver DiseaseImmunology and AllergyKupffer cellsMESH: AnimalsCell Self RenewalMESH: Lipid MetabolismMice KnockoutKupffer cellLipidsResearch Highlightmacrophages[SDV] Life Sciences [q-bio]Infectious Diseasesmedicine.anatomical_structureLiver030220 oncology & carcinogenesismonocytesmedicine.medical_specialtynon-alcoholic steatohepatitis (NASH)ImmunologyBiology03 medical and health sciencesMESH: Mice Inbred C57BLMESH: Cell ProliferationInternal medicinemedicineAnimalsLiver damageMESH: MiceCell ProliferationMESH: Non-alcoholic Fatty Liver DiseaseTriglyceride storageNon alcoholicLipid Metabolismmedicine.diseaseMESH: Lipidseye diseasesMice Inbred C57BLMESH: Kupffer Cells030104 developmental biologyEndocrinologySteatohepatitisHomeostasisMESH: LiverImmunity
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Autophagy Stimulation as a Potential Strategy Against Intestinal Fibrosis

2019

We recently observed reduced autophagy in Crohn’s disease patients and an anti-inflammatory effect of autophagy stimulation in murine colitis, but both anti- and pro-fibrotic effects are associated with autophagy stimulation in different tissues, and fibrosis is a frequent complication of Crohn’s disease. Thus, we analyzed the effects of pharmacological modulation of autophagy in a murine model of intestinal fibrosis and detected that autophagy inhibition aggravates, while autophagy stimulation prevents, fibrosis. These effects are associated with changes in inflammation and in collagen degradation in primary fibroblasts. Thus, pharmacological stimulation of autophagy may be useful against …

0301 basic medicineautophagyStimulationInflammationDiseaseIntestinal fibrosis03 medical and health sciencesMice0302 clinical medicineCrohn DiseaseFibrosismedicineintestinal fibrosisMurine colitisAnimalslcsh:QH301-705.5Sirolimusbusiness.industryBrief ReportAutophagyGeneral MedicineFibroblastsmedicine.diseaseFibrosisIntestinesMice Inbred C57BLDisease Models Animal030104 developmental biologylcsh:Biology (General)inflammationCancer research030211 gastroenterology & hepatologyCollagenmedicine.symptomComplicationbusinessImmunosuppressive AgentsCells
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Age‐related ultrastructural changes of the basement membrane in the mouse blood‐brain barrier

2018

Abstract The blood‐brain barrier (BBB) is essential for a functional neurovascular unit. Most studies focused on the cells forming the BBB, but very few studied the basement membrane (BM) of brain capillaries in ageing. We used transmission electron microscopy and electron tomography to investigate the BM of the BBB in ageing C57BL/6J mice. The thickness of the BM of the BBB from 24‐month‐old mice was double as compared with that of 6‐month‐old mice (107 nm vs 56 nm). The aged BBB showed lipid droplets gathering within the BM which further increased its thickness (up to 572 nm) and altered its structure. The lipids appeared to accumulate toward the glial side of the BM. Electron tomography …

0301 basic medicineblood‐brain barrierAgingElectron Microscope TomographyMyocytes Smooth Muscleelectron tomographyBlood–brain barrierMuscle Smooth Vascular03 medical and health sciencesMice0302 clinical medicineMicroscopy Electron TransmissionLipid dropletmedicineAnimalsBasement membraneChemistryNeurodegenerationBrainLipid metabolismBiological TransportCell BiologyOriginal ArticlesLipid Dropletsmedicine.diseaseLipid Metabolismbasement membraneCell biologyCapillariesMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureElectron tomographyAgeingageingBlood-Brain Barrier030220 oncology & carcinogenesisAstrocytesUltrastructureMolecular MedicineOriginal ArticleNeuroglia
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A Weaning Reaction to Microbiota Is Required for Resistance to Immunopathologies in the Adult.

2019

International audience; Microbes colonize all body surfaces at birth and participate in the development of the immune system. In newborn mammals, the intestinal microbiota is first shaped by the dietary and immunological components of milk and then changes upon the introduction of solid food during weaning. Here, we explored the reactivity of the mouse intestinal immune system during the first weeks after birth and into adulthood. At weaning, the intestinal microbiota induced a vigorous immune response—a “weaning reaction”—that was programmed in time. Inhibition of the weaning reaction led to pathological imprinting and increased susceptibility to colitis, allergic inflammation, and cancer …

0301 basic medicinecolitis[SDV]Life Sciences [q-bio]short-chain fatty acidsImmunologyRetinoic acidTretinoinWeaningBiologyT-Lymphocytes Regulatoryregulatory T cellsAllergic inflammation03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineImmune systemRAR-related orphan receptor gammamicrobiotamedicineImmunology and AllergyWeaningAnimalsinflammatory pathologyColitisImprinting (psychology)Intestinal Mucosaneonatal periodNuclear Receptor Subfamily 1 Group F Member 3medicine.diseaseFatty Acids Volatile3. Good healthGastrointestinal Microbiome[SDV] Life Sciences [q-bio]Mice Inbred C57BL030104 developmental biologyInfectious DiseaseschemistryAnimals NewbornSolid food030220 oncology & carcinogenesisImmunologymucosal immunityImmunity
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