Search results for " Knockout"

showing 10 items of 764 documents

Effects of Nrf2 deficiency on bone microarchitecture in an experimental model of osteoporosis

2014

Objective. Redox imbalance contributes to bone fragility. We have evaluated the in vivo role of nuclear factor erythroid derived 2-related factor-2 (Nrf2), an important regulator of cellular responses to oxidative stress, in bone metabolism using a model of postmenopausal osteoporosis. Methods. Ovariectomy was performed in both wild-type and mice deficient in Nrf2 (Nrf2-/-). Bone microarchitecture was analyzed by CT. Serum markers of bone metabolism were also measured. Reactive oxygen species production was determined using dihydrorhodamine 123. Results. Sham-operated or ovariectomized Nrf2 -/- mice exhibit a loss in trabecular bone mineral density in femur, accompanied by a reduction in co…

Agingmedicine.medical_specialtycytoarchitectureArticle SubjectNF-E2-Related Factor 2MedicinaOsteoporosisOsteoclastsBone Marrow Cellsprotein deficiencymedicine.disease_causeenvironment and public healthBiochemistryBone resorptionBone remodelingMiceIn vivoInternal medicinemedicineAnimalsFemurcontrolled studyFemurlcsh:QH573-671Cells CulturedMice Knockoutchemistry.chemical_classificationReactive oxygen specieslcsh:CytologyChemistrybone densityCell DifferentiationCell BiologyGeneral Medicinerespiratory systemmedicine.diseaseosteoporosisMice Inbred C57BLDisease Models AnimalOxidative StressEndocrinologyOvariectomized ratReactive Oxygen SpeciesTomography X-Ray ComputedBiomarkersOxidative stressResearch Article
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The Transcription Factor T-bet Is Induced by IL-15 and Thymic Agonist Selection and Controls CD8αα+ Intraepithelial Lymphocyte Development

2014

Summary CD8αα + intraepithelial lymphocytes (IELs) are instrumental in maintaining the epithelial barrier in the intestine. Similar to natural killer cells and other innate lymphoid cells, CD8αα + IELs constitutively express the T-box transcription factor T-bet. However, the precise role of T-bet for the differentiation or function of IELs is unknown. Here we show that mice genetically deficient for T-bet lacked both TCRαβ + and TCRγδ + CD8αα + IELs and thus are more susceptible to chemically induced colitis. Although T-bet was induced in thymic IEL precursors (IELPs) as a result of agonist selection and interleukin-15 (IL-15) receptor signaling, it was dispensable for the generation of IEL…

AgonistCD4-Positive T-Lymphocytesmedicine.drug_classCD8 AntigensReceptors Antigen T-Cell alpha-betaImmunologychemical and pharmacologic phenomenaBiologyCD8-Positive T-Lymphocytesdigestive systemMiceTRANSCRIPTION FACTOR TmedicineTranscriptional regulationImmunology and AllergyAnimalsIntestinal MucosaTranscription factorInterleukin-15Mice KnockoutReceptors Interleukin-15Innate lymphoid cellCell DifferentiationEpithelial CellsReceptors Antigen T-Cell gamma-deltahemic and immune systemsColitisCell biologyIntestinesMice Inbred C57BLInfectious DiseasesInterleukin 15ImmunologyIntraepithelial lymphocyteT-Box Domain ProteinstissuesFunction (biology)Signal TransductionImmunity
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The atypical cannabinoid O-1602 protects against experimental colitis and inhibits neutrophil recruitment.

2011

Background: Cannabinoids are known to reduce intestinal inflammation. Atypical cannabinoids produce pharmacological effects via unidentified targets. We were interested in whether the atypical cannabinoid O-1602, reportedly an agonist of the putative cannabinoid receptor GPR55, reduces disease severity of dextran sulfate sodium (DSS) and trinitrobenzene sulfonic acid (TNBS)-induced colitis in C57BL/6N and CD1 mice. Methods: DSS (2.5% and 4%) was supplied in drinking water for 1 week while TNBS (4 mg) was applied as a single intrarectal bolus. Results: Both treatments caused severe colitis. Injection of O-1602 (5 mg/kg intraperitoneally) significantly reduced macroscopic and histological col…

AgonistMaleCannabinoid receptormedicine.drug_classColonNeutrophilsmedicine.medical_treatmentPharmacologyMotor ActivityInflammatory bowel diseaseArticleReceptors G-Protein-CoupledReceptor Cannabinoid CB2chemistry.chemical_compoundMiceReceptor Cannabinoid CB1CyclohexanesmedicineImmunology and AllergyAnimalsCannabidiolColitisReceptorReceptors CannabinoidPeroxidaseMice KnockoutAnalysis of VarianceO-1602business.industryCannabinoidsDextran SulfateGastroenterologyResorcinolsmedicine.diseaseColitisMice Inbred C57BLChemotaxis LeukocyteDisease Models AnimalchemistryGPR55Neutrophil InfiltrationTrinitrobenzenesulfonic AcidImmunologylipids (amino acids peptides and proteins)CannabinoidbusinessInflammatory bowel diseases
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Biphasic effects of cannabinoids in anxiety responses: CB1 and GABA(B) receptors in the balance of GABAergic and glutamatergic neurotransmission

2012

Biphasic effects of cannabinoids have been shown in processes such as feeding behavior, motor activity, motivational processes and anxiety responses. Using two different tests for the characterization of anxiety-related behavior (elevated plus-maze and holeboard), we first identified in wild-type C57BL/6N mice, two doses of the synthetic CB1 cannabinoid receptor agonist CP-55,940 with anxiolytic (1 mug/kg) and anxiogenic properties (50 mug/kg), respectively. To clarify the role of CB1 receptors in this biphasic effect, both doses were applied to two different conditional CB1 receptor knockout (KO) mouse lines, GABA-CB1-KO (CB1 receptor inactivation in forebrain GABAergic neurons) and Glu-CB…

AgonistMaleCannabinoid receptormedicine.drug_classmedicine.medical_treatmentGlutamic AcidCyclopentanesPharmacologyGABAB receptorBiologyAnxietyMotor ActivityAnxiolyticSynaptic TransmissionGlutamatergicMiceReceptor Cannabinoid CB1medicineAnimalsGABA Agonistsgamma-Aminobutyric AcidPharmacologyMice KnockoutBehavior AnimalDose-Response Relationship DrugCannabinoidsfood and beveragesCyclohexanolsMice Inbred C57BLPsychiatry and Mental healthPyrimidinesAnxiogenicnervous systemReceptors GABA-BGABAergiclipids (amino acids peptides and proteins)Original ArticleCannabinoidpsychological phenomena and processes
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CB1 cannabinoid receptor-mediated aggressive behavior

2013

This study examined the role of cannabinoid CB1 receptors (CB1r) in aggressive behavior. Social encounters took place in grouped and isolated mice lacking CB1r (CB1KO) and in wild-type (WT) littermates. Cognitive impulsivity was evaluated in the delayed reinforcement task (DRT). Gene expression analyses of monoaminooxidase-A (MAO-A), catechol-o-methyl-transferase (COMT), 5-hydroxytriptamine transporter (5-HTT) and 5-HT1B serotonergic receptor (5HT1Br) in the median and dorsal raphe nuclei (MnR and DR, respectively) and in the amygdala (AMY) were performed by real time-PCR. Double immunohistochemistry studies evaluated COMT and CB1r co-localization in the raphe nuclei and in the cortical (AC…

AgonistMalemedicine.medical_specialtyCannabinoid receptorTime Factorsmedicine.drug_classmedicine.medical_treatmentPoison controlArachidonic AcidsSerotonergicCatechol O-MethyltransferaseAmygdalaCellular and Molecular NeuroscienceMiceDorsal raphe nucleusReceptor Cannabinoid CB1Internal medicinemedicineAnimalsInterpersonal RelationsMonoamine OxidasePharmacologyCannabinoid Receptor AgonistsMice KnockoutSerotonin Plasma Membrane Transport ProteinsAmygdalaSurgeryAggressionmedicine.anatomical_structureEndocrinologynervous systemGene Expression RegulationImpulsive BehaviorReceptor Serotonin 5-HT1BConditioning OperantRaphe NucleiCannabinoidRaphe nucleiPsychologyReinforcement Psychology
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Methylprednisolone prevents nerve injury-induced hyperalgesia in neprilysin knockout mice.

2013

The pathophysiology of the complex regional pain syndrome involves enhanced neurogenic inflammation mediated by neuropeptides. Neutral endopeptidase (neprilysin, NEP) is a key enzyme in neuropeptide catabolism. Our previous work revealed that NEP knock out (ko) mice develop more severe hypersensitivity to thermal and mechanical stimuli after chronic constriction injury (CCI) of the sciatic nerve than wild-type (wt) mice. Because treatment with glucocorticoids is effective in early complex regional pain syndrome, we investigated whether methylprednisolone (MP) reduces pain and sciatic nerve neuropeptide content in NEP ko and wt mice with nerve injury. After CCI, NEP ko mice developed more se…

Agonistmedicine.medical_specialtymedicine.drug_classNeuropeptideSubstance PMethylprednisolonechemistry.chemical_compoundMiceInternal medicineMedicineAnimalsNeprilysinMice KnockoutNeurogenic inflammationbusiness.industryfungiNerve injuryMice Inbred C57BLAnesthesiology and Pain MedicineEndocrinologyNeuroprotective AgentsNeurologychemistryHyperalgesiaAnesthesiaHyperalgesiaNeprilysinNeurology (clinical)Sciatic nervemedicine.symptomSciatic NeuropathybusinessPainReferences
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Altered atypical coupling of γ-aminobutyrate type A receptor agonist and convulsant binding sites in subunit-deficient mouse lines

2001

We searched for subunit correlations for GABA(A) receptor-associated atypically GABA-insensitive [35S]TBPS binding. The homomeric beta3 subunit receptors could be excluded, as GABA-insensitive [35S]TBPS binding was present in beta3-/- mice. Localization of GABA-insensitive [35S]TBPS binding correlated best with those of delta, alpha4 and alpha6 subunit mRNAs. The amounts of GABA-insensitive [35S]TBPS binding components were increased in delta-/- mice, but dramatically reduced in alpha6-/- mice, suggesting a role for alpha6 but excluding delta subunits.

Agonistmedicine.medical_specialtymedicine.drug_classProtein subunitMolecular Sequence DataConvulsantsBiologySulfur Radioisotopesmedicine.disease_causeMiceRadioligand AssayCellular and Molecular NeuroscienceInternal medicinemedicineAnimalsHomomericRNA MessengerBinding siteReceptorGABA AgonistsMolecular BiologyBrain ChemistryMice KnockoutMutationBinding SitesGABAA receptorBridged Bicyclo Compounds HeterocyclicReceptors GABA-AMolecular biologyEndocrinologynervous systemConvulsantMolecular Brain Research
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Assessment of mechanisms driving non-linear dose-response relationships in genotoxicity testing.

2014

In genetic toxicology, risk assessment has traditionally adopted linear dose-responses for any compound that causes genotoxic effects. Increasing evidence of non-linear dose-responses, however, suggests potential cellular tolerance to low levels of many genotoxicants with diverse modes of action. Such putative non-linear dose-responses need to be substantiated by strong mechanistic data that identifies the mechanisms responsible for the tolerance to low doses. This can be achieved by experimental demonstration of cytoprotective mechanisms and by providing experimental support for the existence of tolerance mechanisms against low dose effects. By highlighting key experiments into low dose me…

Alkylating AgentsDNA repairmedicine.drug_classTopoisomerase InhibitorsHealth Toxicology and MutagenesisTransgeneComputational biologyBiologyRisk AssessmentGenotoxicity testingToxicologyGeneticsmedicineAnimalsHumansGene knockoutDose-Response Relationship DrugMutagenicity TestsLow doseNucleosidesAneugensOxidantsModels ChemicalParticulate MatterTopoisomerase inhibitorGenetic ToxicologyDNA DamageMutagensMutation research. Reviews in mutation research
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Primary mouse fibroblasts deficient for c-Fos, p53 or for both proteins are hypersensitive to UV light and alkylating agent-induced chromosomal break…

2000

The important regulatory proteins, c-Fos and p53 are induced by exposure of cells to a variety of DNA damaging agents. To investigate their role in cellular defense against genotoxic compounds, we comparatively analysed chromosomal aberrations and apoptosis induced by ultraviolet (UV-C) light and the potent alkylating agent methyl methanesulfonate (MMS) in primary diploid mouse fibroblasts knockout for either c-Fos or p53, or double knockout for both genes. We show that c-Fos and p53 deficient fibroblasts are more sensitive than the corresponding wild-type cells as to the induction of chromosomal aberrations and apoptosis. Double knockout fibroblasts lacking both c-Fos and p53 are viable an…

Alkylating AgentsUltraviolet RaysDNA repairDNA damageHealth Toxicology and MutagenesisDrug ResistanceMutagenesis (molecular biology technique)ApoptosisBiologyRadiation ToleranceCell LineMicechemistry.chemical_compoundGeneticsAnimalsMolecular BiologyGene knockoutChromosome AberrationsMice KnockoutGenes fosFibroblastsCell cycleGenes p53Molecular biologyMethyl methanesulfonatechemistryApoptosisCell cultureTumor Suppressor Protein p53Proto-Oncogene Proteins c-fosDNA DamageMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Interruption of CD28-mediated costimulation during allergen challenge protects mice from allergic airway disease

2012

Background Allergic asthma is a T H 2-promoted hyperreactivity with an immediate, IgE, and mast cell–dependent response followed by eosinophil-dominated inflammation and airway obstruction. Objective Because costimulation by CD28 is essential for T H 2 but not T H 1 responses, we investigated the effect of selective interference with this pathway in mice using the models of ovalbumin and house dust mite–induced airway inflammation. Methods To study the role of CD28 in the effector phase of allergic airway inflammation, we developed an inducibly CD28-deleting mouse strain or alternatively used a CD28 ligand-binding site–specific mouse anti-mouse mAb blocking CD28 engagement. Results We show …

Allergic asthmaLymphocyte ActivationImmunoglobulin Emedicine.disease_causeT-Lymphocytes RegulatoryMice0302 clinical medicineAirway resistanceAllergenImmunology and AllergySensitizationMice Inbred BALB C0303 health sciencesbiologyAntibodies Monoclonalovalbuminrespiratory system3. Good healthmedicine.anatomical_structurecostimulationconditional CD28 knockout miceFemalemedicine.symptomImmunologyInflammation03 medical and health sciencesTh2 CellsCD28 AntigensRespiratory HypersensitivitymedicineAnimalsHumansAntigens DermatophagoidesLymphocyte CountAntibodies Blocking030304 developmental biologyHouse dust miteCD28-specific mAbbusiness.industryReceptor Cross-TalkAirway obstructionmedicine.diseasebiology.organism_classificationMice Mutant Strainsrespiratory tract diseasesDisease Models AnimalCTLA-4Immunologybiology.proteinbusiness030215 immunology
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