Search results for "C57BL"

showing 10 items of 1292 documents

Duodenal contractile activity in dystrophic (mdx) mice: reduction of nitric oxide influence.

2003

The present study was undertaken to analyse duodenal contractility in adult dystrophic (mdx) mice. The spontaneous changes of the isometric tension and the responses of longitudinal duodenal muscle to nonadrenergic, noncholinergic (NANC) nerve stimulation and to exogenous drugs were compared between normal and mdx mice. Duodenal segments from mdx mice displayed spontaneous contractions with higher frequency than normals. N omega-nitro-L-arginine methyl ester (L-NAME) increased the frequency of contractions in normals without affecting that in mdx mice. In normals, NANC nerve stimulation elicited a transient relaxation abolished by L-NAME. In mdx mice a frank relaxation was not observed, the…

musculoskeletal diseasesMalemedicine.medical_specialtyNerve stimulationPhysiologyDuodenumInhibitory pathwayIsometric exerciseIn Vitro TechniquesInhibitory postsynaptic potentialNitric OxideSettore BIO/09 - FisiologiaNitric oxideContractilityDystrophinchemistry.chemical_compoundMiceSmooth muscleInternal medicinemedicineSpontaneous contractionAnimalsNeuroscience (all)biologyDose-Response Relationship DrugEndocrine and Autonomic SystemsIntestinal relaxationGastroenterologymusculoskeletal systemMice Inbred C57BLEndocrinologychemistrybiology.proteinMice Inbred mdxmdx miceSodium nitroprussideDystrophinGastrointestinal Motilitytissuesmedicine.drugMuscle ContractionNeurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
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Combined effect of AAV-U7-induced dystrophin exon skipping and soluble activin Type IIB receptor in mdx mice.

2012

Adeno-associated virus (AAV)-U7-mediated skipping of dystrophin-exon-23 restores dystrophin expression and muscle function in the mdx mouse model of Duchenne muscular dystrophy. Soluble activin receptor IIB (sActRIIB-Fc) inhibits signaling of myostatin and homologous molecules and increases muscle mass and function of wild-type and mdx mice. We hypothesized that combined treatment with AAV-U7 and sActRIIB-Fc may synergistically improve mdx muscle function. Bioactivity of sActRIIB-Fc on skeletal muscle was first demonstrated in wild-type mice. In mdx mice we show that AAV-U7-mediated dystrophin restoration improved specific muscle force and resistance to eccentric contractions when applied a…

musculoskeletal diseasesmdx mousemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesDuchenne muscular dystrophyActivin Receptors Type IIGenetic VectorsMyostatinBiologyDystrophin03 medical and health sciencesMice0302 clinical medicineInternal medicineGeneticsmedicineMyocyteAnimalsMuscular dystrophyMuscle SkeletalMolecular Biology030304 developmental biology0303 health sciencesBody WeightSkeletal muscleExonsGenetic TherapyDependovirusMuscular Dystrophy Animalmedicine.diseasemusculoskeletal system3. Good healthMice Inbred C57BLEndocrinologymedicine.anatomical_structureImmunologybiology.proteinMice Inbred mdxMolecular MedicineITGA7Dystrophin030217 neurology & neurosurgeryMuscle ContractionHuman gene therapy
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Increased dosage of Ink4/Arf protects against glucose intolerance and insulin resistance associated with aging

2013

Recent genome-wide association studies have linked type-2 diabetes mellitus to a genomic region in chromosome 9p21 near the Ink4/Arf locus, which encodes tumor suppressors that are up-regulated in a variety of mammalian organs during aging. However, it is unclear whether the susceptibility to type-2 diabetes is associated with altered expression of the Ink4/Arf locus. In the present study, we investigated the role of Ink4/Arf in age-dependent alterations of insulin and glucose homeostasis using Super-Ink4/Arf mice which bear an extra copy of the entire Ink4/Arf locus. We find that, in contrast to age-matched wild-type controls, Super-Ink4/Arf mice do not develop glucose intolerance with agi…

p16ink4amedicine.medical_specialtyAgingGlucose uptakemedicine.medical_treatmentMice TransgenicCarbohydrate metabolismCDKN2BMiceCDKN2AInsulin resistanceInsulin receptor substrateInternal medicineDiabetes mellitusinsulin resistanceGlucose IntolerancemedicineGlucose homeostasisAnimalsInsulininsulin signalingCyclin-Dependent Kinase Inhibitor p16biologydiabetesADP-Ribosylation FactorsInsulin18F-fluorodeoxyglucose-PETARFCell Biologypancreatic isletmedicine.diseaseMice Inbred C57BLInsulin receptorEndocrinologyGlucosebiology.proteinInsulin Resistancep15ink4bGenome-Wide Association Study
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Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS.

2005

Phosphorylated p38 mitogen-activated protein kinase (p38MAPK), but not activated c-jun-N-terminal kinase (JNK), increases in the motor neurons of transgenic mice overexpressing ALS-linked SOD1 mutants at different stages of the disease. This effect is associated with a selective increase of phosphorylated MKK3-6, MKK4 and ASK1 and a concomitant upregulation of the TNFalpha receptors (TNFR1 and TNFR2), but not IL1beta and Fas receptors. Activation of both p38 MAPK and JNK occurs in the activated microglial cells of SOD1 mutant mice at the advanced stage of the disease; however, this effect is not accompanied by the concomitant activation of the upstream kinases ASK1 and MKK3,4,6, while both …

p38 mitogen-activated protein kinasesMAP Kinase Kinase 3Mice TransgenicMAP Kinase Kinase 6BiologyMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein KinasesReceptors Tumor Necrosis FactorCellular and Molecular NeuroscienceMiceSuperoxide Dismutase-1Downregulation and upregulationAnimalsHumansASK1RNA Messengerfas ReceptorPhosphorylationReceptorProtein kinase AMolecular BiologyP38MAPK cascadeMotor NeuronsKinaseSuperoxide DismutaseTumor Necrosis Factor-alphaAmyotrophic Lateral SclerosisJNK Mitogen-Activated Protein KinasesReceptors Interleukin-1Cell BiologyCell biologyEnzyme ActivationMice Inbred C57BLDisease Models AnimalTumor Necrosis Factor Decoy ReceptorsSpinal CordReceptors Tumor Necrosis Factor Type IDisease ProgressionTumor necrosis factor alphaSignal TransductionMolecular and cellular neurosciences
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Endoderm development requires centrioles to restrain p53-mediated apoptosis in the absence of ERK activity

2021

Centrioles comprise the heart of centrosomes, microtubule-organizing centers. To study the function of centrioles in lung and gut development, we genetically disrupted centrioles throughout the mouse endoderm. Surprisingly, removing centrioles from the endoderm did not disrupt intestinal growth or development but blocked lung branching. In the lung, acentriolar SOX2-expressing airway epithelial cells apoptosed. Loss of centrioles activated p53, and removing p53 restored survival of SOX2-expressing cells, lung branching, and mouse viability. To investigate how endodermal p53 activation specifically killed acentriolar SOX2-expressing cells, we assessed ERK, a prosurvival cue. ERK was active t…

p53Cell SurvivalApoptosisInbred C57BLMedical and Health SciencesArticleGeneral Biochemistry Genetics and Molecular BiologyMiceMorphogenesis2.1 Biological and endogenous factorsAnimalscentrioleintestine developmentAetiologyExtracellular Signal-Regulated MAP KinasesendodermLungMolecular BiologyCentriolesSOXB1 Transcription FactorsStem CellsEndodermapoptosisEpithelial CellsCell BiologyBiological SciencesIntestinesMice Inbred C57BLlung branchingERKembryonic structuresTumor Suppressor Protein p53Microtubule-Associated ProteinsDevelopmental BiologyDevelopmental Cell
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Physical inactivity increases oxidative stress, endothelial dysfunction, and atherosclerosis.

2005

Objective— Sedentary lifestyle is associated with increased cardiovascular events. The underlying molecular mechanisms are incompletely understood. Reactive oxygen species (ROS) contribute to endothelial dysfunction and atherosclerosis. An important source of vascular ROS is the NADPH oxidase. Methods and Results— C57BL6 mice were subjected to regular housing (physical inactivity) or voluntary training on running wheels (6 weeks). Inactivity increased vascular lipid peroxidation to 148±9% and upregulated superoxide release to 176±17% (L-012 chemiluminescence) and 188±29% (cytochrome C reduction assay), respectively. ROS production was predominantly increased in the endothelium and the medi…

rac1 GTP-Binding Proteinmedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIArteriosclerosisNitric Oxide Synthase Type IIBiologymedicine.disease_causechemistry.chemical_compoundMiceApolipoproteins EInternal medicinePhysical Conditioning AnimalmedicineAnimalsNADH NADPH OxidoreductasesRNA MessengerEndothelial dysfunctionLife Stylechemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseSuperoxideNeuropeptidesNADPH Oxidase 1NADPH Oxidasesmedicine.diseasePhosphoproteinsMice Mutant Strainsrac GTP-Binding ProteinsMice Inbred C57BLVasodilationOxidative Stressmedicine.anatomical_structureEndocrinologychemistryNOX1biology.proteinNADPH Oxidase 1Endothelium VascularNitric Oxide SynthaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressArteriosclerosis, thrombosis, and vascular biology
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Enterobacter cloacae administration induces hepatic damage and subcutaneous fat accumulation in high-fat diet fed mice.

2018

Accumulating evidence indicates that gut microbiota plays a significant role in obesity, insulin resistance and associated liver disorders. Family Enterobacteriaceae and especially Enterobacter cloacae strain B29 have been previously linked to obesity and hepatic damage. The underlying mechanisms, however, remain unclear. Therefore, we comprehensively examined the effects of E. cloacae subsp. cloacae (ATCC® 13047™) administration on host metabolism of mice fed with high-fat diet (HFD). C57BL/6N mice were randomly divided into HFD control, chow control, and E. cloacae treatment groups. The E. cloacae treatment group received live bacterial cells in PBS intragastrically twice a week, every ot…

rasvahapotPathology and Laboratory Medicinerasvat (orgaaniset yhdisteet)ruokavaliotBiochemistryMiceAnimal CellsFibrosislcsh:ScienceImmune ResponseConnective Tissue CellsChemical Reactionsta3141ta3142Lipids3. Good healthPhysical sciencesAdiponectinCellular Typesmedicine.medical_specialtyfatsLipolysisImmunologySubcutaneous FatrasvakudoksetMonomers (Chemistry)glycerolDiet High-Fatta311103 medical and health sciencesSigns and SymptomsEnterobacter cloacaeLipolysisPolymer chemistrylcsh:RBiology and Life SciencesHypertrophymedicine.diseaseReceptor InsulinMice Inbred C57BLBiological Tissue030104 developmental biologyEndocrinologylihavuuslcsh:QGlycerol0301 basic medicinePhysiologyLiver cytologysuolistomikrobistolcsh:MedicineAdipose tissueGut floraMedicine and Health SciencesAdipocytesenterobakteerit2. Zero hungerrasvatMultidisciplinarygastrointestinal microbiotatulehdusbiologyHydrolysisadipose tissueChemistryPhysiological ParametersLiverConnective Tissueembryonic structuresFemaleAnatomymedicine.symptomResearch Articleanimal structuresadipocytesInflammationInsulin resistanceEnterobacteriaceaeDiagnostic MedicineInternal medicinemedicineAnimalsObesityTriglyceridesNutritionurogenital systembusiness.industryBody WeightCell Biologybiology.organism_classificationDietToll-Like Receptor 5Gene Expression RegulationinflammationlipolysisdietbusinessEnterobacter cloacaePLoS ONE
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Maturation of Epidermal Langerhans Cells In Vitro Is Accompanied by Downregulation of 4F2 (CD98) as Determined by Differential Display

1998

Following short-term culture, Langerhans cells mature morphologically and functionally into potent immunostimulatory cells. As regulation of gene expression accompanies this maturation process, it is likely that differentially expressed genes are involved in the maturation events. Using the recently described method of differential display, we generated cDNA expression patterns starting with mRNA of murine epidermal Langerhans cells isolated either directly (fLC) or following 3 d cultivation (cLC). Five hundred putative differentially expressed cDNA fragments were recovered from the gel. For a part of the fragments differential expression was confirmed by dot blot and Southern hybridization…

skinLangerhans cellDNA ComplementaryDown-RegulationFusion Regulatory Protein-1GrowthDermatologyBiologyBiochemistryMiceDownregulation and upregulationAntigens CDComplementary DNAmedicineAnimalsRNA MessengerCloning Moleculardifferential gene expressionGeneMolecular BiologySouthern blotRegulation of gene expressionJNK2Differential displayMice Inbred BALB Cepidermal cellsGene Expression Regulation DevelopmentalCell BiologyMolecular biologyMice Inbred C57BLmedicine.anatomical_structureGenesCell cultureLangerhans CellsAntigens SurfaceCarrier ProteinsSequence AnalysisJournal of Investigative Dermatology
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Dexamethasone premedication suppresses vaccine-induced immune responses against cancer

2020

ABSTRACT Glucocorticosteroids (GCS) have an established role in oncology and are administered to cancer patients in routine clinical care and in drug development trials as co-medication. Given their strong immune-suppressive activity, GCS may interfere with immune-oncology drugs. We are developing a therapeutic cancer vaccine, which is based on a liposomal formulation of tumor-antigen encoding RNA (RNA-LPX) and induces a strong T-cell response both in mice as well as in humans. In this study, we investigated in vivo in mice and in human PBMCs the effect of the commonly used long-acting GCS Dexamethasone (Dexa) on the efficacy of this vaccine format, with a particular focus on antigen-specif…

t-cell primingPremedicationmedicine.medical_treatmentImmunologyPriming (immunology)dexamethasoneglucocorticosteroidsProinflammatory cytokineMice03 medical and health sciences0302 clinical medicineImmune systemAntigenCancer immunotherapyNeoplasmsAnimalsHumansImmunology and AllergyMedicineRC254-282Original ResearchMice Inbred BALB Ccancer immunotherapybusiness.industryrna vaccineImmunityNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC581-607Mice Inbred C57BLCytokineOncology030220 oncology & carcinogenesisImmunologyt-cell vaccineFemaleCancer vaccineImmunologic diseases. AllergybusinessT-cell vaccineResearch Article030215 immunologyOncoImmunology
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The prolyl-isomerase PIN1 is essential for nuclear Lamin-B structure and function and protects heterochromatin under mechanical stress.

2021

Summary: Chromatin organization plays a crucial role in tissue homeostasis. Heterochromatin relaxation and consequent unscheduled mobilization of transposable elements (TEs) are emerging as key contributors of aging and aging-related pathologies, including Alzheimer’s disease (AD) and cancer. However, the mechanisms governing heterochromatin maintenance or its relaxation in pathological conditions remain poorly understood. Here we show that PIN1, the only phosphorylation-specific cis/trans prolyl isomerase, whose loss is associated with premature aging and AD, is essential to preserve heterochromatin. We demonstrate that this PIN1 function is conserved from Drosophila to humans and prevents…

transposonsNeocortexMiceHeterochromatinProlyl isomeraseDrosophila ProteinsBiology (General)PhosphorylationRNA Small InterferingTissue homeostasisCells CulturedSettore ING-INF/05 - Sistemi Di Elaborazione Delle InformazioniNeuronsLamin Type BChemistryHP1phosphorylationneurodegenerationnuclear envelopePeptidylprolyl IsomeraseCell biologyDrosophila heterochromatin HP1 Lamin mechanical stress neurodegeneration nuclear envelope phosphorylation PIN1 transposonsNuclear laminaDrosophilaRNA InterferencePremature agingQH301-705.5HeterochromatinNuclear EnvelopeDrosophila; heterochromatin; HP1; Lamin; mechanical stress; neurodegeneration; nuclear envelope; phosphorylation; PIN1; transposonsSettore BIO/11 - Biologia MolecolareSettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyPIN1Alzheimer DiseaseSettore MED/05 - Patologia ClinicaAnimalsHumansHeterochromatin maintenancemechanical stressheterochromatinmechanical streMice Inbred C57BLNIMA-Interacting Peptidylprolyl IsomeraseChromobox Protein Homolog 5DNA Transposable ElementsHeterochromatin protein 1Stress MechanicalLaminLaminCell reports
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