Search results for "Mouse"

showing 10 items of 590 documents

Neuroprotective effect of Fn14 deficiency is associated with induction of the granulocyte-colony stimulating factor (G-CSF) pathway in experimental s…

2010

Using a transgenic mouse model of ischemic stroke we checked for a possible interaction of antiphospholipid antibodies (aPL) which often cause thromboses as well as central nervous system (CNS) involvement under non-thrombotic conditions and the TWEAK/Fn14 pathway known to be adversely involved in inflammatory and ischemic brain disease. After 7 days, infarct volumes were reduced in Fn14 deficient mice and were further decreased by aPL treatment. This was associated with strongest increase of the endogenous neuroprotective G-CSF/G-CSF receptor system. This unexpected beneficial action of aPL is an example for a non-thrombogenic action and the double-edged nature of aPL.

MaleGenetically modified mouseImmunologyMice TransgenicBiologyNeuroprotectionReceptors Tumor Necrosis FactorBrain IschemiaMiceRandom AllocationTissue factorimmune system diseasesAntiphospholipid syndromeGranulocyte Colony-Stimulating FactormedicineAnimalsHumansImmunology and AllergyneoplasmsStrokeLupus anticoagulantmedicine.diseaseMice Inbred C57BLDisease Models AnimalNeurologyTWEAK ReceptorReceptors Granulocyte Colony-Stimulating FactorImmunologyAntibodies AntiphospholipidTumor necrosis factor alphaNeurology (clinical)Inflammation MediatorsGranulocyte colony-stimulating factor receptorSignal TransductionJournal of Neuroimmunology
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4-Epidoxycycline: an alternative to doxycycline to control gene expression in conditional mouse models

2004

Since the pioneering work by Gossen and Bujard in 1992 demonstrating the usefulness of the Escherichia coli derived tet resistance operon for regulating gene expression a large collection of doxycycline-controlled transgenic mice has been established. Gene switching in eukaryotic tissue culture cells or mice requires administration of tetracycline, anhydrotetracycline or doxycycline to efficiently inactivate the transactivator protein tTA (TET-OFF system) or alternatively to activate the reverse transactivator protein rtTA (TET-ON system). However, the antibiotic activity of doxycycline can create an imbalance of the intestinal flora, resulting in diarrhoea and in a smaller number of animal…

MaleGenetically modified mouseReceptor ErbB-2TransgeneBiophysicsAdministration OralMice NudeAntineoplastic AgentsBreast NeoplasmsMice TransgenicBiologyPharmacologyBiochemistryMiceTransactivationCell Line TumorGene expressionmedicineAnimalsMolecular BiologyDoxycyclineRegulation of gene expressionDose-Response Relationship DrugOncogeneStereoisomerismCell BiologyRatsGene Expression Regulation NeoplasticDisease Models AnimalTreatment OutcomeTetracyclinesCell cultureDoxycyclineImmunologyNIH 3T3 Cellsmedicine.drugBiochemical and Biophysical Research Communications
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Extensive characterization of the human DDAH1 transgenic mice

2009

Abstract Purpose of the research Overexpression of the human dimethylarginine dimethylaminohydrolase type 1 (hDDAH1) gene was reported to have beneficial cardiovascular effects in mice. To date, it is unclear whether these effects are related to enhanced metabolic clearance of asymmetric dimethylarginine (ADMA) and l - N G -mono-methyl- l -arginine ( l -NMMA) or increased DDAH1 expression and activity in cardiovascular tissues of hDDAH1 transgenic mice. Principal results DDAH activity (DDAH1 + DDAH2) was found to be markedly increased in aortic and heart tissues but unaltered in liver and kidney tissues of hDDAH1 transgenic as compared to wild-type (WT) mice. In WT mice, DDAH activity was m…

MaleGenetically modified mousemedicine.medical_specialtyEndotheliumArginineTransgeneMice TransgenicArginineNitric OxideGene Expression Regulation EnzymologicAmidohydrolasesMicechemistry.chemical_compoundEnosInternal medicinemedicineAnimalsHumansTissue DistributionRNA MessengerPharmacologyKidneybiologyChemistryArteriosclerosismedicine.diseasebiology.organism_classificationIsoenzymesMice Inbred C57BLmedicine.anatomical_structureEndocrinologyOrgan SpecificityFemaleAsymmetric dimethylarginineSignal TransductionPharmacological Research
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Esr, a second locus in the house mouse controlling esterase-5

1982

Electrophoretic variation characterized by the presence (ES-5B+) or absence (ES-5B−) of esterase-5B in the plasma of the house mouse has been observed. It is suggested that the expression of esterase-5B is controlled by an autosomal locus, Esr, linked to Ldr-1 on chromosome 6, in addition to the presumptive structural locus Es-5, which is located on chromosome 8. A gene order of Lyt-3-Esr-Ldr-1 was determined by two crosses.

MaleGeneticsGenetic LinkageEsterasesChromosome MappingGenes RecessiveLocus (genetics)General MedicineBiologybiology.organism_classificationBiochemistryMolecular biologyEsteraseHouse mouseMiceGene Expression RegulationGenesGenes RegulatorGeneticsAnimalsFemaleStructural locusMolecular BiologyGeneEcology Evolution Behavior and SystematicsBiochemical Genetics
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Mechanisms underlying the inhibitory effects induced by pituitary adenylate cyclase-activating peptide in mouse ileum

2005

Abstract The aim of this study was to investigate the signal transduction mechanisms underlying the inhibitory effect induced by pituitary adenylate cyclase activating peptide (PACAP-27) on the spontaneous contractile activity of longitudinal muscle of mouse ileum. Mechanical activity of ileal segments was recorded isometrically in vitro. PACAP-27 produced apamin-sensitive reduction of the amplitude of the spontaneous contractions. 9-(Tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536), adenylate cyclase inhibitor, or genistein and tyrphostin 25, tyrosine kinase inhibitors, had negligible effects on PACAP-27-induced inhibition. PACAP-27 effects were significantly inhibited by U-73122, phopho…

MaleIndolesPhosphodiesterase InhibitorsVasodilator AgentsMouse ileumStimulationSettore BIO/09 - FisiologiaMicechemistry.chemical_compoundInositolEnzyme InhibitorsEstrenesRyanodineRyanodine receptorProtein-Tyrosine KinasesTyrphostinsGenisteinPyrrolidinonesCell biologyPituitary adenylate cyclase-activating peptideNG-Nitroarginine Methyl EsterPituitary Adenylate Cyclase-Activating PolypeptideThapsigarginSignal transductionCyclopiazonic acidhormones hormone substitutes and hormone antagonistsMuscle ContractionBoron Compoundsendocrine systemmedicine.medical_specialtyThapsigarginMuscular inhibitionCalcium-Transporting ATPasesIn Vitro TechniquesInositol 145-triphosphateBiologyPACAP-27 (pituitary adenylate cyclase activating peptide)IleumPhospholipase CInternal medicinemedicineAnimalsPharmacologyDose-Response Relationship DrugPhospholipase CAdenineMuscle SmoothMice Inbred C57BLEndocrinologyApaminchemistryAdenylyl Cyclase InhibitorsCalciumNitric Oxide SynthaseEuropean Journal of Pharmacology
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Inflammation-Induced Alteration of Astrocyte Mitochondrial Dynamics Requires Autophagy for Mitochondrial Network Maintenance

2013

Accumulating evidence suggests that changes in the metabolic signature of astrocytes underlie their response to neuroinflammation, but how proinflammatory stimuli induce these changes is poorly understood. By monitoring astrocytes following acute cortical injury, we identified a differential and region-specific remodeling of their mitochondrial network: while astrocytes within the penumbra of the lesion undergo mitochondrial elongation, those located in the core-the area invaded by proinflammatory cells-experience transient mitochondrial fragmentation. In brain slices, proinflammatory stimuli reproduced localized changes in mitochondrial dynamics, favoring fission over fusion. This effect w…

MaleLipopolysaccharidesPhysiologyDnm1l protein mouseInterleukin-1betaNitric Oxide Synthase Type IIMitochondrionAstrocytes/metabolismMitochondrial DynamicsAutophagy-Related Protein 7Mice0302 clinical medicinemetabolism [Reactive Oxygen Species]PhosphorylationCells Culturedcytology [Astrocytes]0303 health sciencesmetabolism [Inflammation]metabolism [Astrocytes]Inflammation/metabolismCytokines/metabolismdrug effects [Mitochondria]Mitochondria/drug effectsMitochondriaCell biologyAstrocytes/drug effectsmedicine.anatomical_structureMicrotubule-Associated Proteins/metabolismPhosphorylationCytokinesmetabolism [Dynamins]Nitric Oxide Synthase Type II/metabolismMicrotubule-Associated ProteinsAstrocytegenetics [Microtubule-Associated Proteins]DynaminsProgrammed cell deathAstrocytes/cytologydrug effects [Astrocytes]Mice TransgenicBiologypharmacology [Interferon-gamma]Proinflammatory cytokine03 medical and health sciencesInterferon-gammametabolism [Interleukin-1beta]reactive astrocytesReactive Oxygen Species/metabolismddc:570Mitochondria/metabolismtoxicity [Lipopolysaccharides]medicineAutophagyAnimalsAutophagy-Related Protein 7Molecular BiologyNeuroinflammation030304 developmental biologypathology [Inflammation]Dynamins/metabolismInflammationdrug effects [Mitochondrial Dynamics]Autophagymetabolism [Cytokines]Interferon-gamma/pharmacologyCell Biologymetabolism [Microtubule-Associated Proteins]Microtubule-Associated Proteins/geneticsMitochondrial Dynamics/drug effectsmetabolism [Mitochondria]metabolism [Nitric Oxide Synthase Type II]Mice Inbred C57BLLipopolysaccharides/toxicityAtg7 protein mouseAstrocytesInterleukin-1beta/metabolismReactive Oxygen Species030217 neurology & neurosurgeryInflammation/pathologyCell Metabolism
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Development of mouse testis and epididymis following intrauterine exposure to a static magnetic field

1999

In order to test if the in utero exposure to static magnetic fields affects testis and epididymis development in mice, females were exposed to 0.5–0.7 T, generated by a permanent magnet, from day 7 of gestation to the day of birth. No significant differences were found between exposed and sham-exposed animals with respect to body weight gain of dam during the gestational period, litter size, body weight of male pups at the day of birth, and body or testis-epididymis weight gain of pups from birth to day 35. Histopathologic evaluation of testis and epididymis of pups of 1, 5, 15, and 35 days of age showed no detectable alterations due to in utero exposure to static magnetic fields. Bioelectr…

MaleLitter (animal)Agingmedicine.medical_specialtyLitter SizePhysiologyBiophysicsMice Inbred StrainsBiologyWeight GainMouse TestisAndrologyMagneticsMicePregnancyInternal medicineTestismedicineAnimalsRadiology Nuclear Medicine and imagingIntrauterine exposureEpididymisHistologyOrgan SizeGeneral MedicineEpididymisEndocrinologymedicine.anatomical_structureAnimals NewbornIn uteroPrenatal Exposure Delayed EffectsGestationFemalemedicine.symptomWeight gain
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Dephosphorylation of p-ERK1/2 in relation to tumor remission after HER-2 and Raf1 blocking therapy in a conditional mouse tumor model

2006

Several studies have shown that HER-2/neu (erbB-2) blocking therapy strategies can cause tumor remission. However, the responsible molecular mechanisms are not yet known. Both ERK1/2 and Akt/PKB are critical for HER-2-mediated signal transduction. Therefore, we used a mouse tumor model that allows downregulation of HER-2 in tumor tissue by administration of anhydrotetracycline (ATc). Switching-off HER-2 caused a rapid tumor remission by more than 95% within 7 d of ATc administration compared to the volume before switching-off HER-2. Interestingly, HER-2 downregulation caused a dephosphorylation of p-ERK1/2 by more than 80% already before tumor remission occurred. Levels of total ERK protein…

MaleMAPK/ERK pathwayCancer Researchmedicine.medical_specialtyReceptor ErbB-2Blotting WesternDown-RegulationMice NudeP erk1 2BiologyTransfectionDephosphorylationMiceDownregulation and upregulationInternal medicinemedicineAnimalsHumansMouse tumorPhosphorylationMolecular BiologyProtein kinase BMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Remission InductionNeoplasms ExperimentalTumor tissueGene Expression Regulation NeoplasticProto-Oncogene Proteins c-rafDisease Models AnimalEndocrinologyTetracyclinesNIH 3T3 CellsCancer researchSignal transductionSignal TransductionMolecular Carcinogenesis
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Blood-brain barrier penetration of the enantiomers of venlafaxine and its metabolites in mice lacking P-glycoprotein

2010

According to in vitro studies the enantiomers of venlafaxine display different degrees of serotonin and noradrenaline reuptake inhibition. Therefore, clarification of the enantiomeric drug distribution between serum and brain is highly warranted. To elucidate if P-glycoprotein (P-gp) in a stereoselective manner transports venlafaxine and its metabolites out of the brain we used abcb1ab double-knockout mice that do not express P-gp. A single dose of racemic venlafaxine (10 mg/kg bw) was intraperitoneally injected to knockout (-/-) and wildtype (+/+) mice. Serum and brain samples were collected 1, 3, 6 and 9 h following drug administration for analysis by LC/MS/MS. One to six hours post-dose,…

MaleMedicin och hälsovetenskapVenlafaxinePharmacologyBlood–brain barrierMedical and Health SciencesMicemedicineAnimalsPharmacology (medical)ATP Binding Cassette Transporter Subfamily B Member 1Biological PsychiatryP-glycoproteinPharmacologyMice KnockoutbiologyChemistryVenlafaxine HydrochlorideBiological TransportStereoisomerismCyclohexanolsIn vitroPsychiatry and Mental healthmedicine.anatomical_structureNeurologyBlood-Brain BarrierKnockout mousebiology.proteinStereoselectivityNeurology (clinical)SerotoninEnantiomerSelective Serotonin Reuptake Inhibitorsmedicine.drug
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Altered brain concentrations of citalopram and escitalopram in P-glycoprotein deficient mice after acute and chronic treatment

2013

Background: According to both in vitro and in vivo data P-glycoprotein (P-gp) may restrict the uptake of several antidepressants into the brain, thus contributing to the poor success rate of current antidepressant therapies. The therapeutic activity of citalopram resides in the Senantiomer, whereas the R-enantiomer is practically devoid of serotonin reuptake potency. To date, no in vivo data are available that address whether the enantiomers of citalopram and its metabolites are substrates of P-gp. Methods: P-gp knockout (abcb1ab (-/-)) and wild-type (abcb1ab (+/+)) mice underwent acute (single-dose) and chronic (two daily doses for 10 days) treatment with citalopram (10 mg/kg) or escitalop…

MaleMedicin och hälsovetenskapescitalopramenantiomersCitaloprammice knockoutP-glycoproteinCitalopramPharmacologyMedical and Health Sciencesbehavioral disciplines and activitiesMiceIn vivomental disordersmedicineAnimalsEscitalopramPotencyPharmacology (medical)ATP Binding Cassette Transporter Subfamily B Member 1Biological PsychiatryP-glycoproteinMice KnockoutPharmacologybiologybusiness.industryBrainPsychiatry and Mental healthNeurologyKnockout mousebiology.proteinAntidepressive Agents Second-GenerationAntidepressantNeurology (clinical)Enantiomerbusinessmedicine.drugEuropean Neuropsychopharmacology
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