Search results for "Knockout"

showing 10 items of 806 documents

Platelet-localized FXI promotes a vascular coagulation-inflammatory circuit in arterial hypertension

2017

Multicellular interactions of platelets, leukocytes, and the blood vessel wall support coagulation and precipitate arterial and venous thrombosis. High levels of angiotensin II cause arterial hypertension by a complex vascular inflammatory pathway that requires leukocyte recruitment and reactive oxygen species production and is followed by vascular dysfunction. We delineate a previously undescribed, proinflammatory coagulation-vascular circuit that is a major regulator of vascular tone, blood pressure, and endothelial function. In mice with angiotensin II-induced hypertension, tissue factor was up-regulated, as was thrombin-dependent endothelial cell vascular cellular adhesion molecule 1 ex…

Blood PlateletsMale0301 basic medicinemedicine.medical_specialtyMacrophage-1 AntigenVascular Cell Adhesion Molecule-1Blood Pressure030204 cardiovascular system & hematologyThromboplastinMice03 medical and health sciencesTissue factor0302 clinical medicineThrombinInternal medicinemedicineAnimalsHumansPlateletRats WistarEndothelial dysfunctionBlood CoagulationFactor XIAgedMice Knockoutbusiness.industryAngiotensin IIThrombinGeneral MedicineMiddle AgedOligonucleotides Antisensemedicine.diseaseAngiotensin IIMice Inbred C57BL030104 developmental biologyEndocrinologyBlood pressuremedicine.anatomical_structurePlatelet Glycoprotein GPIb-IX ComplexPathophysiology of hypertensionHypertensionFemalebusinessmedicine.drugBlood vesselScience Translational Medicine
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Pharmacokinetics of acute and sub-chronic aripiprazole in P-glycoprotein deficient mice

2010

Abstract Background P-glycoprotein (P-gp), an efflux transporter localized in the blood–brain barrier, limits the access of multiple xenobiotics to the central nervous system (CNS). For the new antipsychotic aripiprazole and its active metabolite dehydroaripiprazole differences in disposition in blood and brain were investigated after acute and sub-chronic administration in a P-gp knockout mouse model. Methods Serum and brain concentrations of both drugs were measured at several time points 1–24 h after i.p. injection of 10 mg/kg aripiprazole and after 11 days of sub-chronic administration in several tissues. Moreover, the expression of P-gp was determined by Western blot analysis after sub…

Blotting WesternCentral nervous systemAripiprazoleQuinolonesPharmacologyBlood–brain barrierMass SpectrometryPiperazinesMiceCellular and Molecular NeurosciencePharmacokineticsmedicineAnimalsATP Binding Cassette Transporter Subfamily B Member 1Chromatography High Pressure LiquidActive metaboliteP-glycoproteinMice KnockoutPharmacologyAnalysis of VariancebiologyChemistryBrainBiological TransportTransportermedicine.anatomical_structureBlood-Brain BarrierKnockout mousebiology.proteinAripiprazoleAntipsychotic Agentsmedicine.drugNeuropharmacology
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3-D image analysis of fluorescent drug binding

2004

Fluorescent ligands provide the means of studying receptors in whole tissues using confocal laser scanning microscopy and have advantages over antibody- or non-fluorescence-based method. Confocal microscopy provides large volumes of images to be measured. Histogram analysis of 3-D image volumes is proposed as a method of graphically displaying large amounts of volumetric image data to be quickly analyzed and compared. The fluorescent ligand BODIPY FL-prazosin (QAPB) was used in mouse aorta. Histogram analysis reports the amount of ligand-receptor binding under different conditions and the technique is sensitive enough to detect changes in receptor availability after antagonist incubation or…

Boron CompoundsMalelcsh:Medical technologyAdrenergic receptorBiomedical EngineeringMouse aortaIn Vitro TechniquesAntibodieslaw.inventionMiceImaging Three-DimensionalConfocal microscopylawReceptors Adrenergic alpha-1HistogramAnimalsRadiology Nuclear Medicine and imagingReceptorlcsh:QH301-705.5Adrenergic alpha-AntagonistsAortaFluorescent DyesMice KnockoutMicroscopy ConfocalDose-Response Relationship DrugPhenoxybenzamineChemistryPrazosinBiological tissueCondensed Matter PhysicsFluorescenceAutofluorescencelcsh:Biology (General)lcsh:R855-855.5BiophysicsMolecular MedicineFemaleBiotechnology
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The Cytokine GM-CSF Drives the Inflammatory Signature of CCR2+ Monocytes and Licenses Autoimmunity.

2015

Granulocyte-macrophage colony-stimulating factor (GM-CSF) has emerged as a crucial cytokine produced by auto-reactive T helper (Th) cells that initiate tissue inflammation. Multiple cell types can sense GM-CSF, but the identity of the pathogenic GM-CSF-responsive cells is unclear. By using conditional gene targeting, we systematically deleted the GM-CSF receptor (Csf2rb) in specific subpopulations throughout the myeloid lineages. Experimental autoimmune encephalomyelitis (EAE) progressed normally when either classical dendritic cells (cDCs) or neutrophils lacked GM-CSF responsiveness. The development of tissue-invading monocyte-derived dendritic cells (moDCs) was also unperturbed upon Csf2r…

CCR2Myeloidmedicine.medical_treatmentInterleukin-1betaAutoimmunitymedicine.disease_causeMonocytesAutoimmunityCytokine Receptor Common beta Subunit0302 clinical medicineSTAT5 Transcription FactorImmunology and AllergyAntigens LyMyeloid CellsPhosphorylationMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionExperimental autoimmune encephalomyelitisGene targetingFlow CytometryInfectious DiseasesCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factor2723 Immunology and Allergymedicine.symptommedicine.drugSignal TransductionEncephalomyelitis Autoimmune ExperimentalReceptors CCR2Immunology610 Medicine & healthInflammationMice TransgenicBiology03 medical and health sciencesmedicineAnimalsHumans030304 developmental biologyInflammation2403 ImmunologyGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesDendritic Cellsmedicine.disease10040 Clinic for NeurologyImmunologyTranscriptome030217 neurology & neurosurgery
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Impact of Glutathione Peroxidase-1 Deficiency on Macrophage Foam Cell Formation and Proliferation: Implications for Atherogenesis

2013

Clinical and experimental evidence suggests a protective role for the antioxidant enzyme glutathione peroxidase-1 (GPx-1) in the atherogenic process. GPx-1 deficiency accelerates atherosclerosis and increases lesion cellularity in ApoE(-/-) mice. However, the distribution of GPx-1 within the atherosclerotic lesion as well as the mechanisms leading to increased macrophage numbers in lesions is still unknown. Accordingly, the aims of the present study were (1) to analyze which cells express GPx-1 within atherosclerotic lesions and (2) to determine whether a lack of GPx-1 affects macrophage foam cell formation and cellular proliferation. Both in situ-hybridization and immunohistochemistry of l…

CD36 AntigensMAPK/ERK pathwayMouseMitogen-Activated Protein Kinase 3lcsh:MedicineGene ExpressionSignal transductionCardiovascularMiceMolecular cell biologyGlutathione Peroxidase GPX1lcsh:ScienceIn Situ HybridizationFoam cellMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MultidisciplinaryReverse Transcriptase Polymerase Chain ReactionKinaseSignaling cascadesScavenger Receptors Class AAnimal ModelsImmunohistochemistryLipoproteins LDLMedicineFemaleSignal transductionResearch ArticleMacrophage colony-stimulating factorMAPK signaling cascadesBlotting WesternBiologyCell GrowthModel OrganismsApolipoproteins EVascular BiologyAnimalsHumansProtein kinase ABiologyCell ProliferationGlutathione PeroxidaseMacrophage Colony-Stimulating Factorlcsh:RAtherosclerosisMolecular biologyMacrophages Peritoneallcsh:QMacrophage proliferationFoam CellsPLoS ONE
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CD36 is involved in lycopene and lutein uptake by adipocytes and adipose tissue cultures

2011

International audience; Scope: Carotenoids are mainly stored in adipose tissue. However, nothing is known regarding the uptake of carotenoids by adipocytes. Thus, our study explored the mechanism by which lycopene and lutein, two major human plasma carotenoids, are transported. Methods and results: CD36 was a putative candidate for this uptake, 3T3-L1 cells were treated with sulfosuccinimidyl oleate, a CD36-specific inhibitor. sulfosuccinimidyl oleate-treated cells showed a significant decrease in both lycopene and lutein uptake as compared to control cells. Their uptake was also decreased by partial inhibition of CD36 expression using siRNA, whereas the overexpression of CD36 in Cos-1 cell…

CD36 AntigensMaleLutein030309 nutrition & dieteticsCD36[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionLYCOPENEAdipose tissueOleic Acidschemistry.chemical_compoundMiceChlorocebus aethiopsRNA Small InterferingCAROTENOIDSCarotenoidComputingMilieux_MISCELLANEOUSchemistry.chemical_classificationMice KnockoutGENE CD360303 health sciencesbiologyCD 36food and beveragesLycopene3. Good healthADIPOCYTESADIPOSE TISSUEBiochemistryCOS CellsRNA InterferenceBiotechnologyAdipose tissue macrophagesAdipose Tissue WhiteSuccinimides03 medical and health sciencesOrgan Culture Techniques3T3-L1 CellsTRANSPORTEUR BIOLOGIQUEparasitic diseasesAnimalsHumans030304 developmental biologyBiological Transport[SDV.AEN] Life Sciences [q-bio]/Food and NutritionGLYCOPROTEINRchemistryLUTEINbiology.protein[SDV.AEN]Life Sciences [q-bio]/Food and NutritionEx vivoFood ScienceExplant culture
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Luminal Lipid Regulates CD36 Levels and Downstream Signaling to Stimulate Chylomicron Synthesis

2011

International audience; The membrane glycoprotein CD36 binds nanomolar concentrations of long chain fatty acids (LCFA) and is highly expressed on the luminal surface of enterocytes. CD36 deficiency reduces chylomicron production through unknown mechanisms. In this report, we provide novel insights into some of the underlying mechanisms. Our in vivo data demonstrate that CD36 gene deletion in mice does not affect LCFA uptake and subsequent esterification into triglycerides by the intestinal mucosa exposed to the micellar LCFA concentrations prevailing in the intestine. In rodents, the CD36 protein disappears early from the luminal side of intestinal villi during the postprandial period, but …

CD36 AntigensMaleMTPCD36[SDV]Life Sciences [q-bio]BiochemistryMicrosomal triglyceride transfer proteinMice0302 clinical medicineIntestinal mucosaCricetinaeChylomicronsLipoproteinHypertriglyceridemiaMice Knockout0303 health sciencesMitogen-Activated Protein Kinase 3biologyPostprandial PeriodLipid-binding ProteinIntestineApoB48ERKmedicine.anatomical_structurePostprandialBiochemistrylipids (amino acids peptides and proteins)Apolipoprotein B-48MAP Kinase Signaling SystemEnterocyteCHO CellsChylomicron03 medical and health sciencesCricetulusparasitic diseasesmedicineAnimalsRats WistarMolecular Biology030304 developmental biologyUbiquitinationLipid absorptionLipid metabolismCell BiologyLipid MetabolismRatsEnterocytesMetabolismbiology.proteinApolipoprotein B-48CD36[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryChylomicron
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The Lipid-Sensor Candidates CD36 and GPR120 Are Differentially Regulated by Dietary Lipids in Mouse Taste Buds: Impact on Spontaneous Fat Preference

2011

BACKGROUND: Recent studies in rodents and humans suggest that the chemoreception of long-chain fatty acids (LCFA) in oral cavity is involved in the spontaneous preference for fatty foods and might contribute to the obesity risk. CD36 and GPR120 are LCFA receptors identified in rodent taste bud cells. The fact that CD36 or GPR120 gene inactivation leads to a decrease in the preference for lipids raises the question of the respective role(s) played by these gustatory lipid-sensor candidates. METHODOLOGY/PRINCIPAL FINDINGS: Using a combination of biochemical, nutritional and behavioural studies in wild-type, CD36(+/-)and CD36(-/-) mice, it was found that: 1°) CD36 and GPR120 display different …

CD36 AntigensMaleTasteChemoreceptorAnatomy and PhysiologyRodentCD36Blotting Westernlcsh:MedicineGene ExpressionReal-Time Polymerase Chain ReactionReceptors G-Protein-CoupledFood PreferencesMicebiology.animalIntegrative PhysiologyGene expressionAnimalsObesityReceptorlcsh:ScienceGeneBiologyNutritionMice KnockoutMultidisciplinarybiologylcsh:RGPR120Taste BudsDietary FatsImmunohistochemistrySensory SystemsCircadian RhythmBiochemistrybiology.proteinMedicinelipids (amino acids peptides and proteins)lcsh:QResearch ArticlePLoS ONE
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Upregulation of liver VLDL receptor and FAT/CD36 expressions in LDLR-/- apoB100/100 mice fed trans-10,cis-12 conjugated linoleic acid

2006

International audience; This study explores the mechanisms responsible for the fatty liver setup in mice fed trans-10,cis-12 conjugated linoleic acid (t10c12 CLA), hypothesizing that an induction of low density lipoprotein receptor (LDLR) expression is associated with lipid accumulation. To this end, the effects of t10c12 CLA treatment on lipid parameters, serum lipoproteins, and expression of liver lipid receptors were measured in LDLR(-/-) apoB(100/100) mice as a model of human familial hypercholesterolemia itself depleted of LDLR. Mice were fed t10c12 CLA over 2 or 4 weeks. We first observed that the treatment induced liver steatosis, even in the absence of LDLR. Mice treated for 2 weeks…

CD36 AntigensMaleVery low-density lipoproteinTRANSLOCASECD36RECEPTEUR SCAVENGER[SDV]Life Sciences [q-bio]FATTY ACID TRANSLOCASE030204 cardiovascular system & hematologyBiochemistryMice0302 clinical medicineEndocrinologyLinoleic Acids ConjugatedMice Knockout0303 health sciencesLipoprotein lipaselipoprotéinebiologyacide grasrécepteur d'hormoneChemistryFatty liverFatty Acidsfood and beveragesHEPATIC LIPASELipidsLOW DENSITY LIPOPROTEIN RECEPTOR3. Good healthUp-RegulationLiverSCAVENGER RECEPTOR CLASS B TYPE ILIVER STEATOSIS;LOW DENSITY LIPOPROTEIN RECEPTOR;TRIGLYCERIDE;LIPOATROPHY;LIPOPROTEIN;FATTY ACID TRANSLOCASE;VERY LOW DENSITY LIPOPROTEIN RECEPTOR;HEPATIC LIPASE;LIPOPROTEIN LIPASE;LOW DENSITY LIPOPROTEIN RECEPTOR-RELATED PROTEIN;SCAVENGER RECEPTOR CLASS B TYPE I;LIPOATROPHIE;TRANSLOCASE;LIPASE HEPATIQUE;RECEPTEUR SCAVENGERApolipoprotein B-100lipoprotéine lipaseTRIGLYCERIDElipids (amino acids peptides and proteins)Oxidation-Reductionmedicine.medical_specialtyLIPASE HEPATIQUELipolysisVLDL receptorMice Transgenicacide linoléique conjugué03 medical and health sciencesstéatose hépatiqueInternal medicineLIVER STEATOSISmedicineLIPOPROTEIN LIPASEAnimalsRNA Messengerlipoprotéine de faible densite030304 developmental biologyLOW DENSITY LIPOPROTEIN RECEPTOR-RELATED PROTEINnutritional and metabolic diseasesCell Biologymedicine.diseaseLipid MetabolismLIPOATROPHYDietary FatsEndocrinologyLIPOPROTEINReceptors LDLVERY LOW DENSITY LIPOPROTEIN RECEPTORLIPOATROPHIELDL receptorbiology.proteinacide gras transHepatic lipaseLipoprotein
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Cylindromatosis (Cyld) gene mutation in T cells promotes the development of an IL-9-dependent allergic phenotype in experimental asthma

2016

Cylindromatosis (CYLD) is a ubiquitously expressed deubiquitinating enzyme which removes activating ubiquitin residues from important signaling molecules of the NF-κB pathway. In CYLDex7/8 transgenic mice, a naturally occurring short isoform (sCYLD) is overexpressed in the absence of full length CYLD, leading to excessive NF-κB activity. Herein, we investigated the impact of the CYLDex7/8 mutation selectively in T cells on the development of experimental allergic airway disease induced by sensitization and challenge with ovalbumin. Compared with their wildtype littermates, mice bearing the T cell-specific mutation (CD4+CYLDex7/8) display stronger eosinophilia and mucus production in the lun…

CD4-Positive T-Lymphocytes0301 basic medicineSkin Neoplasmsmedicine.medical_treatmentT cellImmunologyGene mutationImmunoglobulin Emedicine.disease_causeTh9 cellsDeubiquitinating enzymeMice03 medical and health sciencesNeoplastic Syndromes HereditaryHypersensitivitymedicineAnimalsHumansSensitizationMice KnockoutMutationbiologyTumor Suppressor ProteinsInterleukin-9Cylindromatosis (turban tumor syndrome) geneIL-9AsthmaDeubiquitinating Enzyme CYLDEosinophilsMice Inbred C57BLMucusOvalbumin030104 developmental biologymedicine.anatomical_structureCytokineModels AnimalMutationImmunologybiology.proteinCellular Immunology
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