Search results for "mouse model"

showing 10 items of 84 documents

Hematopoietic Stem Cells Reversibly Switch from Dormancy to Self-Renewal during Homeostasis and Repair

2008

Bone marrow hematopoietic stem cells (HSCs) are crucial to maintain lifelong production of all blood cells. Although HSCs divide infrequently, it is thought that the entire HSC pool turns over every few weeks, suggesting that HSCs regularly enter and exit cell cycle. Here, we combine flow cytometry with label-retaining assays (BrdU and histone H2B-GFP) to identify a population of dormant mouse HSCs (d-HSCs) within the lin(-)Sca1(+)cKit(+)CD150(+)CD48(-)CD34(-) population. Computational modeling suggests that d-HSCs divide about every 145 days, or five times per lifetime. d-HSCs harbor the vast majority of multilineage long-term self-renewal activity. While they form a silent reservoir of th…

BromouracilProliferationCellCD34CELLCYCLEQuiescenceSelf renewalMice0302 clinical medicineLongBone MarrowHomeostasisCancereducation.field_of_study0303 health sciencesProgenitor Cellshemic and immune systemsCell cycleCell biologyAdult Stem CellsHaematopoiesismedicine.anatomical_structure030220 oncology & carcinogenesisFluorouracilStem cellGreen Fluorescent ProteinsPopulationMice TransgenicCycleBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesmedicineAnimalsProgenitor celleducationUridine030304 developmental biologyMouse ModelBiochemistry Genetics and Molecular Biology(all)Osteoblastic NicheHematopoietic Stem CellsSTEMCELLAntigens DifferentiationMarrowIn-VitroImmunologyDormancyBone marrowHomeostasisCell
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Expression of stress protein gp96, a tumor rejection antigen, in human colorectal cancer

2000

Preparations of stress protein gp96 from tumor cells are active as tumor vaccines by eliciting immune responses against mixtures of individual tumor peptide antigens which are complexed to gp96. Due to the individual antigenicity of tumors, a vaccine consisting of tumor-derived gp96 has to be prepared individually for each patient from autologous tumor tissue. So far, gp96 expression by human tumors has not been analyzed. Here, we report stable and mostly homogenous expression of gp96 by colorectal cancer, which was enhanced compared to surrounding tumor stroma in 70% to 80% of colorectal cancer specimens. Fewer non-metastatic than metastatic primary cancer specimens showed enhanced gp96 ex…

CA15-3Cancer ResearchColorectal cancerbusiness.industryTumor M2-PKMouse model of colorectal and intestinal cancermedicine.diseaseImmunohistochemistryNeoplasm ProteinsImmune systemOncologyAntigenCell cultureImmunologymedicineHumansCA19-9Colorectal NeoplasmsbusinessHT29 CellsHeat-Shock ProteinsInternational Journal of Cancer
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Mesenchymal stromal-cell transplants induce oligodendrocyte progenitor migration and remyelination in a chronic demyelination model.

2013

Demyelinating disorders such as leukodystrophies and multiple sclerosis are neurodegenerative diseases characterized by the progressive loss of myelin that may lead toward a chronic demyelination of the brain’s white matter, impairing normal axonal conduction velocity and ultimately causing neurodegeneration. Current treatments modifying the pathological mechanisms are capable of ameliorating the disease; however, frequently, these therapies are not sufficient to repress the progressive demyelination into a chronic condition and permanent loss of function. To this end, we analyzed the effect that bone marrow-derived mesenchymal stromal cell (BM-MSC) grafts exert in a chronically demyelinate…

Cancer ResearchPathologymedicine.medical_specialtyNeurogenesisImmunologyNeural ConductionBiologyMesenchymal Stem Cell TransplantationModels Biologicaltrophic releaseCuprizoneMiceCellular and Molecular NeuroscienceMyelinNerve FibersCell MovementmedicineSubependymal zoneAnimalsNerve Growth FactorsStem Cell NicheProgenitor cellRemyelinationMyelin Sheathdemyelinating mouse modelMultiple sclerosisMesenchymal stem cellCell DifferentiationMesenchymal Stem CellsCell Biologymedicine.diseaseAxonsOligodendrocyteTransplantationDisease Models AnimalOligodendrogliaremyelinationmedicine.anatomical_structureChronic DiseaseDentate GyrusImmunologyoligodendrocyte activationOriginal Articlemesenchymal stromal cellsGenèticaDemyelinating Diseases
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URINARY TRACT OBSTRUCTION AND REDUCED NEPHRON NUMBER: ADAPTATION OF NEPHRONS FOLLOWED THROUGH ADULTHOOD IN A MOUSE MODEL

2015

Congenital urinary tract obstruction , NEPHRON NUMBER, MOUSE MODEL , release of obstruction

Congenital urinary tract obstruction NEPHRON NUMBER MOUSE MODEL release of obstruction
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In vivo fate mapping with SCL regulatory elements identifies progenitors for primitive and definitive hematopoiesis in mice.

2009

10 páginas, 6 figuras.-- et al.

Definitive hematopoiesisEmbryologyMyeloidPopulationConditional mouse modelIn vivo linage and fate tracingEmbryonic DevelopmentStem cell leukemia geneBiology03 medical and health sciencesMice0302 clinical medicineFate mappinghemic and lymphatic diseasesProto-Oncogene ProteinsCRE systemmedicineBasic Helix-Loop-Helix Transcription FactorsAnimalsCell LineageMesodermal blood cell specificationGene Knock-In TechniquesProgenitor celleducationGeneTetracycline systemT-Cell Acute Lymphocytic Leukemia Protein 1Primitive hematopoiesis030304 developmental biology0303 health scienceseducation.field_of_studyMicroscopy ConfocalStem CellsEmbryoFlow CytometryCell biologyHematopoiesisGastrulationHaematopoiesismedicine.anatomical_structureBlood cell precursors030220 oncology & carcinogenesisImmunologyIn vivo lineage markingDevelopmental BiologyMechanisms of development
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Deletion of myosin VI causes slow retinal optic neuropathy and age-related macular degeneration (AMD)-relevant retinal phenotype

2015

The unconventional myosin VI, a member of the actin-based motor protein family of myosins, is expressed in the retina. Its deletion was previously shown to reduce amplitudes of the a- and b-waves of the electroretinogram. Analyzing wild-type and myosin VI-deficient Snell’s Waltzer mice in more detail, the expression pattern of myosin VI in retinal pigment epithelium, outer limiting membrane, and outer plexiform layer could be linked with differential progressing ocular deficits. These encompassed reduced a-waves and b-waves and disturbed oscillatory potentials in the electroretinogram, photoreceptor cell death, retinal microglia infiltration, and formation of basal laminar deposits. A pheno…

Genotypegenetic structuresOuter retinaTranslocator protein TSPOOuter plexiform layermacromolecular substancesBiologyRetinaPhotoreceptor cellMouse modelStereociliaMacular DegenerationMiceCellular and Molecular Neurosciencechemistry.chemical_compoundOptic Nerve DiseasesMyosinmedicineAnimalsBipolar cellMolecular BiologyPharmacologyRetinaRetinal pigment epitheliumMyosin Heavy ChainsNeurodegenerationInner retinaChoriocapillarisRetinalCell BiologyAnatomyMacular degenerationmedicine.diseaseSynapseeye diseasesCell biologyMice Inbred C57BLmedicine.anatomical_structurechemistryMolecular MedicineMicrogliasense organsGene DeletionResearch ArticlePhotoreceptor Cells VertebrateCellular and Molecular Life Sciences
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Non-alcoholic fatty pancreas disease pathogenesis: a role for developmental programming and altered circadian rhythms.

2013

Objectives Emerging evidence suggests that maternal obesity (MO) predisposes offspring to obesity and the recently described non-alcoholic fatty pancreas disease (NAFPD) but involved mechanisms remain unclear. Using a pathophysiologically relevant murine model, we here investigated a role for the biological clock - molecular core circadian genes (CCG) in the generation of NAFPD. Design Female C57BL6 mice were fed an obesogenic diet (OD) or standard chow (SC) for 6 weeks, prior to pregnancy and throughout gestation and lactation: resulting offspring were subsequently weaned onto either OD (Ob_Ob and Con_Ob) or standard chow (Ob_Con and Con_Con) for 6 months. Biochemical, pro-inflammatory and…

HeredityPhysiologylcsh:MedicineCLOCK ProteinsGene ExpressionMouse ModelsGastroenterology and HepatologyResearch and Analysis MethodsModel OrganismsPregnancyGeneticsMedicine and Health SciencesAnimalsRNA MessengerObesitylcsh:ScienceNutritionAnalysis of Variancelcsh:RBody WeightGene Expression Regulation DevelopmentalPancreatic DiseasesBiology and Life SciencesAnimal ModelsCircadian RhythmMice Inbred C57BLPhysiological ParametersPrenatal Exposure Delayed Effectslcsh:QFemaleEpigeneticsAnatomyPhysiological ProcessesDigestive SystemChronobiologyResearch ArticlePloS one
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Blocking Activin Receptor Ligands Is Not Sufficient to Rescue Cancer-Associated Gut Microbiota—A Role for Gut Microbial Flagellin in Colorectal Cance…

2019

Colorectal cancer (CRC) and cachexia are associated with the gut microbiota and microbial surface molecules. We characterized the CRC-associated microbiota and investigated whether cachexia affects the microbiota composition. Further, we examined the possible relationship between the microbial surface molecule flagellin and CRC. CRC cells (C26) were inoculated into mice. Activin receptor (ACVR) ligands were blocked, either before tumor formation or before and after, to increase muscle mass and prevent muscle loss. The effects of flagellin on C26-cells were studied in vitro. The occurrence of similar phenomena were studied in murine and human tumors. Cancer modulated the gut microbiota witho…

INTERLEUKIN-6suolistomikrobisto3122 CancersmicrobiomeENTEROCOCCUS-FAECALISlcsh:RC254-282ArticlePATHWAYACTIVATIONMOUSE MODELSIL-6 EXPRESSIONpaksusuolisyöpätulehdusCOLON-CANCERactivinliganditlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensIL6inflammationmyostatinSKELETAL-MUSCLEproteiinitlihassurkastumasairaudetTUMOR MICROENVIRONMENTCCL2MCP-1Cancers
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Correction: Recovery from Toxic-Induced Demyelination Does Not Require the NG2 Proteoglycan.

2018

[This corrects the article DOI: 10.1371/journal.pone.0163841.].

ImmunologyGene ExpressionMouse ModelsCell MigrationResearch and Analysis MethodsPathology and Laboratory MedicineCorpus CallosumDirected Cell MigrationModel OrganismsNerve FibersSigns and SymptomsAnimal CellsDiagnostic MedicineMedicine and Health SciencesGeneticsImmune ResponseNeuronsInflammationChemotaxisBiology and Life SciencesBrainCell DifferentiationAnimal ModelsCell BiologyAxonsCell MotilityCellular NeuroscienceCellular TypesAnatomyResearch ArticleDevelopmental BiologyNeurosciencePloS one
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Mast cells partly contribute to allergic enteritis development: Findings in two different mast cell-deficient mice

2021

Allergic enteritis (AE) is a gastrointestinal form of food allergy. The presence of mast cells and granulocytes has been detected in the inflamed tissues in AE. In this study, we aimed to elucidate the role of mast cells in AE development using two mast cell-deficient mouse strains: KIT(W-sh/W-sh) bearing the W-sash (W(sh)) inversion mutation and Cpa3Cre/+, which lack mast cells due to Cre-mediated mast cell eradication, were used in an AE experimental model. The development of clinical symptoms (e.g. drop in body temperature and weight loss) were abolished in both strains, whereas inflammatory levels of AE (e.g. villous atrophy, edema, and granulocyte accumulation) were reduced mainly in K…

LebensmittelallergieEOSINOPHILImmunologyBiologyFOOD ALLERGYMiceAllergic enteritisHypersensitivityDeficient mousemedicineAnimalsHumansImmunology and AllergyMast CellsMast (botany)ALLERGIC ENTERITISMice KnockoutMAST CELLSMOUSE MODEL//purl.org/becyt/ford/3.1 [https]Mast cellEnteritisMice Inbred C57BLmedicine.anatomical_structureImmunology//purl.org/becyt/ford/3 [https]
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