Search results for "inbred c57bl"

showing 10 items of 1287 documents

Intervention of Inflammatory Monocyte Activity Limits Dermal Fibrosis

2019

Monocytes and monocyte-derived cells are important players in the initiation, progression, and resolution of inflammatory skin reactions. As inflammation is a prerequisite for fibrosis development, we focused on the role of monocytes in cutaneous fibrosis, the clinical hallmark of patients suffering from systemic sclerosis. Investigating the function of monocytes in reactive oxygen species–induced dermal fibrosis, we observed that early monocyte depletion partially reduced disease severity. Low numbers of inflammatory Ly6Chigh monocytes, as well as inhibition of CCR2 and CCL2 in wild type animals by a specific L-RNA aptamer, mitigated disease parameters, indicating a pivotal role for CCR2+ …

0301 basic medicineCCR2Nerve growth factor IBReceptors CCR2InflammationDermatologyCCL2BiochemistryMonocytesSclerodermaMiceRandom Allocation03 medical and health sciences0302 clinical medicineReference ValuesFibrosisNuclear Receptor Subfamily 4 Group A Member 1medicineAnimalsHumansMolecular BiologyCells CulturedChemokine CCL2InflammationScleroderma Systemicbusiness.industryMonocyteInterferon-stimulated geneBiopsy NeedleCell Biologymedicine.diseaseImmunohistochemistryMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureGene Expression Regulation030220 oncology & carcinogenesisImmunologymedicine.symptombusinessSignal TransductionJournal of Investigative Dermatology
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Oleanolic acid improves diet-induced obesity by modulating fat preference and inflammation in mice.

2018

Obesity, triggered by high-fat diet (HFD), is associated to altered gustatory perception of dietary lipids. Oleanolic acid (OLA), a triterpene, has been reported to exert anti-obesity effects in animal models. Hence, we investigated the role of OLA in the modulation of oro-sensory perception of lipids in control and HFD-induced obese mice. As expected, OLA-treated obese mice exhibited a decrease in body, liver, and visceral adipose tissue weights. OLA treatment improved glucose tolerance, insulin level, plasma lipopolysaccharide (LPS), and hepatic cholesterol and triglyceride concentrations. OLA-treated obese mice exhibited higher fat preference compared to untreated obese mice, probably du…

0301 basic medicineCD36 AntigensLipopolysaccharidesmedicine.medical_specialtyCD36medicine.medical_treatmentInterleukin-1betaAdipose tissue030209 endocrinology & metabolismInflammationDiet High-FatDiet MediterraneanWeight GainBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineTaste receptorInternal medicinemedicineAnimalsInsulinObesityRNA MessengerOleanolic AcidCarbohydrate-responsive element-binding proteinOleanolic acidInflammationbiologyTriglycerideChemistryInterleukin-6InsulinLipogenesisGeneral MedicineGlucose Tolerance TestTaste BudsMice Inbred C57BL030104 developmental biologyEndocrinologyAdipose TissueLiverbiology.proteinCalciumFemalemedicine.symptomInflammation MediatorsBiochimie
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EBI2 Is Highly Expressed in Multiple Sclerosis Lesions and Promotes Early CNS Migration of Encephalitogenic CD4 T Cells

2017

Arrival of encephalitogenic T cells at inflammatory foci represents a critical step in development of experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis. EBI2 and its ligand, 7{alpha},25-OHC, direct immune cell localization in secondary lymphoid organs. CH25H and CYP7B1 hydroxylate cholesterol to 7{alpha},25-OHC. During EAE, we found increased expression of CH25H by microglia and CYP7B1 by CNS-infiltrating immune cells elevating the ligand concentration in the CNS. Two critical pro-inflammatory cytokines, interleukin-23 (IL-23) and interleukin-1 beta (IL-1{beta}), maintained expression of EBI2 in differentiating Th17 cells. In line with this, EBI2 enhan…

0301 basic medicineCD4-Positive T-LymphocytesCentral Nervous SystemMaleGPR183Cancer ResearchEncephalomyelitis Autoimmune ExperimentalOxysterolCentral nervous systemInterleukin-1betaCytochrome P450 Family 7CH25HmicrogliaAutoimmunityBiologymedicine.disease_causemultiple sclerosisInterleukin-23General Biochemistry Genetics and Molecular BiologyAutoimmunityReceptors G-Protein-Coupled03 medical and health sciencesMiceImmune systemCell MovementmedicineAnimalsEBI2lcsh:QH301-705.5MicrogliaEAEMultiple sclerosisExperimental autoimmune encephalomyelitisGPR18325-OHCmedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)ImmunologySteroid HydroxylasesTh17 CellsFemaleTh17CNSoxysterolCell Reports
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The iNOS Activity During an Immune Response Controls the CNS Pathology in Experimental Autoimmune Encephalomyelitis

2019

Inducible nitric oxide synthase (iNOS) plays a critical role in the regulation of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Previous studies have shown that iNOS plays pathogenic as well as regulatory roles in MS and EAE. However, how does iNOS alters the pathophysiology of the central nervous system (CNS) in neuronal autoimmunity is not clearly understood. In the present work, we show that treatment of mice with L-NAME, an iNOS inhibitor, during the antigen-priming phase primarily alters brain pathology, while in the subsequent effector phase of the immune response, the spinal cord is involved. Inhibition of iNOS during the priming phase of the immune res…

0301 basic medicineCD4-Positive T-LymphocytesPathologyexperimental autoimmune encephalomyelitisNitric Oxide Synthase Type IIApoptosismedicine.disease_causeAutoimmunityMice0302 clinical medicineImmunology and AllergyEnzyme InhibitorsOriginal ResearchMice KnockoutbiologyExperimental autoimmune encephalomyelitisautoimmunityCell DifferentiationNitric oxide synthaseOligodendrogliamedicine.anatomical_structureNG-Nitroarginine Methyl EsterIntegrin alpha Mlcsh:Immunologic diseases. Allergymedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisLymphoid TissueCentral nervous systemImmunology03 medical and health sciencesInterferon-gammaImmune systemmedicineAnimalsHumansNOS2−/− neuroinflammationNeuroinflammationbusiness.industryMultiple sclerosisinducible nitric oxide synthaseDendritic Cellsmedicine.diseasecentral nervous systemMice Inbred C57BL030104 developmental biologybiology.proteinbusinesslcsh:RC581-607030215 immunologyGranulocytesFrontiers in Immunology
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Reciprocal regulation of the Il9 locus by counteracting activities of transcription factors IRF1 and IRF4.

2017

The T helper 9 (Th9) cell transcriptional network is formed by an equilibrium of signals induced by cytokines and antigen presentation. Here we show that, within this network, two interferon regulatory factors (IRF), IRF1 and IRF4, display opposing effects on Th9 differentiation. IRF4 dose-dependently promotes, whereas IRF1 inhibits, IL-9 production. Likewise, IRF1 inhibits IL-9 production by human Th9 cells. IRF1 counteracts IRF4-driven Il9 promoter activity, and IRF1 and IRF4 have opposing function on activating histone modifications, thus modulating RNA polymerase II recruitment. IRF1 occupancy correlates with decreased IRF4 abundance, suggesting an IRF1-IRF4-binding competition at the I…

0301 basic medicineCD4-Positive T-LymphocytesScienceCellular differentiationAntigen presentationGeneral Physics and AstronomyRNA polymerase IIMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciences0302 clinical medicineInterferonmedicineAnimalsHumansInterleukin 9Transcription factorMice KnockoutMultidisciplinaryGene Expression ProfilingQInterleukin-9Cell DifferentiationGeneral ChemistryT-Lymphocytes Helper-InducerCell biologyMice Inbred C57BL030104 developmental biologyIRF1Interferon Regulatory Factorsbiology.protein030215 immunologyInterferon regulatory factorsmedicine.drugInterferon Regulatory Factor-1Nature communications
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Microenvironments to study migration and somal translocation in cortical neurons

2018

Migrating post-mitotic neurons of the developing cerebral cortex undergo terminal somal translocation (ST) when they reach their final destination in the cortical plate. This process is crucial for proper cortical layering and its perturbation can lead to brain dysfunction. Here we present a reductionist biomaterials platform that faithfully supports and controls the distinct phases of terminal ST in vitro. We developed microenvironments with different adhesive molecules to support neuronal attachment, neurite extension, and migration in distinct manners. Efficient ST occurred when the leading process of migratory neurons crossed from low-to high-adhesive areas on a substrate, promoting spr…

0301 basic medicineCORTICAL NEURONSGrowth ConesBiophysicsCEREBRAL CORTEXBioengineeringINGENIERÍAS Y TECNOLOGÍASBiologySOMAL TRANSLOCATIONMicrotubulesBiotecnología IndustrialBiomaterials03 medical and health sciences0302 clinical medicineMicrotubuleCell MovementmedicineSomal translocationCell AdhesionAnimalsCell adhesionGrowth coneCerebral CortexNeuronsBioproductos Biomateriales Bioplásticos Biocombustibles Bioderivados etc.Cortical neuronsActin cytoskeletonMice Inbred C57BLCORTICOGENESISCorticogenesisActin Cytoskeleton030104 developmental biologymedicine.anatomical_structureCellular MicroenvironmentNEURONAL MIGRATIONMechanics of MaterialsCerebral cortexCeramics and CompositesNeuroscience030217 neurology & neurosurgery
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HMG-CoA reductase promotes protein prenylation and therefore is indispensible for T-cell survival.

2017

AbstractStatins are a well-established family of drugs that lower cholesterol levels via the competitive inhibition of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). In addition, the pleiotropic anti-inflammatory effects of statins on T cells make them attractive as therapeutic drugs in T-cell-driven autoimmune disorders. Since statins do not exclusively target HMGCR and thus might have varying effects on different cell types, we generated a new mouse strain allowing for the tissue-specific deletion of HMGCR. Deletion of HMGCR expression in T cells led to a severe decrease in their numbers with the remaining cells displaying an activated phenotype, with an increased pro…

0301 basic medicineCancer ResearchGeranylgeranyl pyrophosphateCell SurvivalT cellT-LymphocytesImmunologyProtein PrenylationMevalonic AcidCell CountMevalonic acidLymphocyte ActivationT-Lymphocytes Regulatory03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinePolyisoprenyl PhosphatesmedicineAnimalsbiologyCell DeathIntegrasesCholesterolCell BiologyHydroxymethylglutaryl-CoA reductaseCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurePhenotypeBiochemistrychemistryHMG-CoA reductasebiology.proteinProtein prenylationlipids (amino acids peptides and proteins)Hydroxymethylglutaryl CoA ReductasesOriginal ArticleMevalonate pathway030217 neurology & neurosurgeryGene DeletionCell deathdisease
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Nicotinamide Phosphoribosyltransferase Acts as a Metabolic Gate for Mobilization of Myeloid-Derived Suppressor Cells

2019

Abstract Cancer induces alteration of hematopoiesis to fuel disease progression. We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates the myeloid cell levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway, which acts as negative regulator of the CXCR4 retention axis of hematopoietic cells in the bone marrow. NAMPT inhibits CXCR4 through a NAD/Sirtuin 1–mediated inactivation of HIF1α-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide. Pharmacologic inhibition or myeloid-specific ablation …

0301 basic medicineCancer ResearchMyeloidmedicine.medical_treatmentNudeNicotinamide phosphoribosyltransferaseApoptosisColorectal NeoplasmInbred C57BLMicechemistry.chemical_compound0302 clinical medicineTumor Cells CulturedHematopoiesiNicotinamide PhosphoribosyltransferaseInbred BALB CMice Inbred BALB CCulturedbiologySarcomaTumor CellsHaematopoiesismedicine.anatomical_structureOncology030220 oncology & carcinogenesisSirtuinFemaleSarcoma ExperimentalColorectal NeoplasmsAnimals; Apoptosis; Cell Proliferation; Colorectal Neoplasms; Female; Hematopoiesis; Humans; Mammary Neoplasms Experimental; Mice; Mice Inbred BALB C; Mice Inbred C57BL; Mice Nude; Myeloid-Derived Suppressor Cells; NAD; Nicotinamide Phosphoribosyltransferase; Sarcoma Experimental; Signal Transduction; Tumor Cells Cultured; Xenograft Model Antitumor AssaysHumanSignal TransductionMice NudeExperimental03 medical and health sciencesmedicineMyeloid-Derived Suppressor CellAnimalsHumansCell ProliferationAnimalMyeloid-Derived Suppressor CellsMammary NeoplasmsApoptosiMammary Neoplasms ExperimentalImmunotherapyNADXenograft Model Antitumor AssaysHematopoiesisMice Inbred C57BL030104 developmental biologychemistrybiology.proteinCancer researchMyeloid-derived Suppressor CellNAD+ kinaseBone marrowCancer Research
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Morpho-functional study of vascular fluorochrome delivery to lung and liver metastases of Lewis lung carcinoma (3LL).

1991

The growth of 3LL liver and lung metastases related to Its vascular organization was studied by morphological and functional methods, using the Hoechst 33342 fluorescent DNA staining technique. Experimental liver and lung metastases were produced in syngeneic C57BL/6 mice by injection of 3LL tumor cells into a lateral tail vein or into the spleen, respectively. The resulting neoplasms were composed of large cells arranged in sheets with a thin irregularly distributed stroma. Scattered blood vessels with an open or closed lumen were observed within the tumor. Functional study of H33342 diffusion showed a single and reticular fluorescent pattern in liver metastases. In contrast, in lung meta…

0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsLumen (anatomy)SpleenMetastasisMice03 medical and health sciences0302 clinical medicineStromaParenchymamedicineAnimalsFluorescent DyesLung030102 biochemistry & molecular biologybusiness.industryCarcinomaLiver NeoplasmsLewis lung carcinomaGeneral Medicinemedicine.diseaseMice Inbred C57BLPerfusionMicroscopy Electronmedicine.anatomical_structureOncology030220 oncology & carcinogenesisReticular connective tissueBenzimidazolesbusiness
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Persistent immune stimulation exacerbates genetically driven myeloproliferative disorders via stromal remodeling

2017

Abstract Systemic immune stimulation has been associated with increased risk of myeloid malignancies, but the pathogenic link is unknown. We demonstrate in animal models that experimental systemic immune activation alters the bone marrow stromal microenvironment, disarranging extracellular matrix (ECM) microarchitecture, with downregulation of secreted protein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation. These changes were accompanied by a decrease in Treg frequency and by an increase in activated effector T cells. Under these conditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells unfit for normal …

0301 basic medicineCancer ResearchStromal cellMyeloidMice TransgenicVascular RemodelingBiologyInbred C57BLTransgenicMice03 medical and health sciencesMyelogenousMyeloproliferative DisordersmedicineAnimalsHumansMyeloproliferative DisorderAnimals; Cell Proliferation; Humans; Mice; Mice Inbred C57BL; Mice Inbred CBA; Mice Transgenic; Myeloproliferative Disorders; Stromal Cells; Vascular Remodeling; Oncology; Cancer ResearchCell ProliferationMyeloproliferative DisordersAnimalStromal CellInbred CBANeutrophil extracellular trapsmedicine.diseaseMice Inbred C57BLHaematopoiesisLeukemia030104 developmental biologymedicine.anatomical_structureOncologyImmunologyMice Inbred CBABone marrowStromal CellsNucleophosminHuman
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