Search results for " Knockout"

showing 10 items of 764 documents

Role of C-reactive protein in atherogenesis: can the apolipoprotein E knockout mouse provide the answer?

2005

Objective—Human C-reactive protein (CRP) was reported to accelerate atherosclerotic lesion development in male but not in female apolipoprotein E (apoE) knockout mice. Here, mice expressing rabbit CRP (rbCRP) were crossbred onto apoE knockout animals, and the effect on atherogenesis was studied.Methods and Results—Hemolytic complement activity could not be detected in apoE knockout mice. Furthermore, in contrast to human complement, neither rabbit nor human CRP complexed to modified low-density lipoprotein–activated murine complement. At 52 weeks, rbCRP levels were similar in male and female transgenic animals. Serum cholesterol levels were equivalent in female animals irrespective of rbCRP…

Apolipoprotein EMalemedicine.medical_specialtyPathologyRatónTransgeneHypercholesterolemiaMice TransgenicLesionMiceApolipoproteins ESpecies SpecificityInternal medicinemedicineAnimalsHumansTransgenesAortaMice KnockoutbiologyVascular diseaseC-reactive proteinCholesterol LDLComplement System Proteinsmedicine.diseaseAtherosclerosisComplement systemMice Inbred C57BLDisease Models AnimalEndocrinologyC-Reactive ProteinKnockout mousebiology.proteinFemaleDietary ProteinsRabbitsmedicine.symptomCardiology and Cardiovascular MedicineArteriosclerosis, thrombosis, and vascular biology
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Inhibition of endocannabinoid-degrading enzyme fatty acid amide hydrolase increases atherosclerotic plaque vulnerability in mice

2013

The role of endocannabinoids such as anandamide during atherogenesis remains largely unknown. Fatty acid amide hydrolase (FAAH) represents the key enzyme in anandamide degradation, and its inhibition is associated with subsequent higher levels of anandamide. Here, we tested whether selective inhibition of FAAH influences the progression of atherosclerosis in mice. Selective inhibition of FAAH using URB597 resulted in significantly increased plasma levels of anandamide compared to control, as assessed by mass spectrometry experiments in mice. Apolipoprotein E-deficient (ApoE(-/-)) mice were fed a high-fat, cholesterol-rich diet to induce atherosclerotic conditions. Simultaneously, mice recei…

Apolipoprotein Emedicine.medical_specialtyApolipoprotein BNeutrophilsPolyunsaturated Alkamidesmedicine.medical_treatmentIntraperitoneal injectionGene ExpressionArachidonic AcidsDiet High-FatAmidohydrolasesMicechemistry.chemical_compoundApolipoproteins EWestern blotCell MovementSuperoxidesFatty acid amide hydrolaseInternal medicinemedicineAnimalsEnzyme InhibitorsMolecular BiologyMice Knockoutbiologymedicine.diagnostic_testChemistryMacrophagesAnandamideURB597Dietary FatsEndocannabinoid systemPlaque AtheroscleroticEndocrinologyBenzamidesbiology.proteinCarbamatesCardiology and Cardiovascular MedicineEndocannabinoidsJournal of Molecular and Cellular Cardiology
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Deficiency of glutathione peroxidase-1 accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice.

2007

Background— We have recently demonstrated that activity of red blood cell glutathione peroxidase-1 is inversely associated with the risk of cardiovascular events in patients with coronary artery disease. The present study analyzed the effect of glutathione peroxidase-1 deficiency on atherogenesis in the apolipoprotein E-deficient mouse. Methods and Results— Female apolipoprotein E-deficient mice with and without glutathione peroxidase-1 deficiency were placed on a Western-type diet for another 6, 12, or 24 weeks. After 24 weeks on Western-type diet, double-knockout mice (GPx-1 −/− ApoE −/− ) developed significantly more atherosclerosis than control apolipoprotein E-deficient mice. Moreover…

Apolipoprotein Emedicine.medical_specialtyGPX1AntioxidantApolipoprotein Bmedicine.medical_treatmentLipoproteinsApoptosisBlood Pressuremedicine.disease_causeNitric OxideMitochondria HeartMonocyteschemistry.chemical_compoundMiceApolipoproteins EGlutathione Peroxidase GPX1SuperoxidesInternal medicinePeroxynitrous AcidmedicineAnimalsAortaCell Proliferationchemistry.chemical_classificationMice KnockoutReactive oxygen speciesGlutathione PeroxidaseMembranesbiologyGlutathione peroxidaseGlutathioneAtherosclerosisEndocrinologyPhenotypechemistryImmunologybiology.proteinDisease ProgressionFemaleCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidation-ReductionOxidative stressArteriosclerosis, thrombosis, and vascular biology
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Reduced VLDL clearance in ApoeNpc1 mice is associated with increased Pcsk9 and Idol expression and decreased hepatic LDL-receptor levels

2010

Niemann-Pick type C1 (NPC1) promotes the transport of LDL receptor (LDL-R)-derived cholesterol from late endosomes/lysosomes to other cellular compartments. NPC1-deficient cells showed impaired regulation of liver_X receptor (LXR) and sterol regulatory element-binding protein (SREBP) target genes. We observed that Apoe(-/-)Npc1(-/-) mice displayed a marked increase in total plasma cholesterol mainly due to increased VLDL, reflecting decreased clearance. Although nuclear SREBP-2 and Ldlr mRNA levels were increased in Apoe(-/-)Npc1(-/-) liver, LDL-R protein levels were decreased in association with marked induction of proprotein convertase subtilisin/kexin type 9 (Pcsk9) and inducible degrade…

Apolipoprotein EreceptorCholesterol VLDLLDL/metabolismMacrophages Peritoneal/cytologyBiochemistryMiceEndocrinologyhemic and lymphatic diseasesReceptorsOrphan Nuclear Receptors/geneticspolycyclic compoundsnuclear receptorCells CulturedResearch ArticlesLiver X ReceptorsMice KnockoutCulturedSterol Regulatory Element Binding Protein 2/geneticslipoproteinSerine EndopeptidasesIntracellular Signaling Peptides and ProteinsLamin Type AOrphan Nuclear ReceptorsTriglycerides/bloodCholesterolLiverProteins/geneticsKexinlipids (amino acids peptides and proteins)Proprotein ConvertasesProprotein Convertase 9Sterol Regulatory Element Binding Protein 1Niemann-Pick diseaseSterol Regulatory Element Binding Protein 2medicine.medical_specialtyCellsKnockoutUbiquitin-Protein LigasesReceptors LDL/metabolismSerine Endopeptidases/geneticsQD415-436BiologyCholesterol/blooddigestive systemApolipoproteins ELiver/physiologySterol Regulatory Element Binding Protein 1/geneticsNiemann-Pick C1 ProteinInternal medicinemedicineAnimalsPeritoneal/cytologyCholesterol VLDL/metabolismUbiquitin-Protein Ligases/geneticsLiver X receptorTriglyceridesMacrophagesPCSK9Proteinsnutritional and metabolic diseasesVLDL/metabolismLamin Type A/metabolismCell BiologySterol regulatory element-binding proteinEndocrinologyReceptors LDLLDL receptorMacrophages PeritonealSterol regulatory element-binding protein 2atherosclerosisApolipoproteins E/geneticsLipoproteinJournal of Lipid Research
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The matricellular protein SPARC supports follicular dendritic cell networking toward Th17 responses.

2011

Abstract Lymphnode swelling during immune responses is a transient, finely regulated tissue rearrangement, accomplished with the participation of the extracellular matrix. Here we show that murine and human reactive lymph nodes express SPARC in the germinal centres. Defective follicular dendritic cell networking in SPARC-deficient mice is accompanied by a severe delay in the arrangement of germinal centres and development of humoral autoimmunity, events that are linked to Th17 development. SPARC is required for the optimal and rapid differentiation of Th17 cells, accordingly we show delayed development of experimental autoimmune encephalomyelitis whose pathogenesis involves Th17. Not only h…

Autoimmune diseases; Extracellular matrix; Germinal centre reaction; Th17 cellsEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisImmunologyCell CommunicationBiologyfollicular dendritic cellExtracellular matrixAnimals Genetically ModifiedMiceImmune systemSPARC; follicular dendritic cell; Th17Autoimmune diseasemedicinegerminal centre reactionImmunology and AllergyAnimalsHumansautoimmune diseasesOsteonectinMice KnockoutB-LymphocytesCD40Follicular dendritic cellsExperimental autoimmune encephalomyelitisMatricellular proteinGerminal centerSPARCCell Differentiationmedicine.diseaseCell biologyExtracellular MatrixImmunity HumoralMice Inbred C57BLCrosstalk (biology)Disease Models AnimalImmunologybiology.proteinDisease ProgressionTh17 CellsImmunizationMyelin-Oligodendrocyte GlycoproteinTh17autoimmune diseases; extracellular matrix; germinal centre reaction; th17 cellsDendritic Cells FollicularMyelin ProteinsJournal of autoimmunity
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Convergence of Wnt signaling on the HNF4alpha-driven transcription in controlling liver zonation.

2009

Background & Aims: In each hepatocyte, the specific repertoire of gene expression is influenced by its exact location along the portocentrovenular axis of the hepatic lobule and provides a reason for the liver functions compartmentalization defined "metabolic zonation." So far, few molecular players controlling genetic programs of periportal (PP) and perivenular (PV) hepatocytes have been identified; the elucidation of zonation mechanisms remains a challenge for experimental hepatology. Recently, a key role in induction and maintenance of the hepatocyte heterogeneity has been ascribed to Wnt/β-catenin pathway. We sought to clarify how this wide-ranging stimulus integrates with hepatocyte s…

Beta-cateninWnt ProteinCellular differentiationBlotting WesternLiver Stem CellFluorescent Antibody TechniqueMice TransgenicBiologyTransfectionSensitivity and SpecificityAnimals; Blotting Western; Cell Differentiation; Cell Proliferation; Cells Cultured; Fluorescent Antibody Technique; Hepatocyte Nuclear Factor 4; Hepatocytes; Humans; Immunoprecipitation; Mice; Mice Knockout; Mice Transgenic; Reverse Transcriptase Polymerase Chain Reaction; Sensitivity and Specificity; Signal Transduction; Transfection; Wnt Proteins; beta Catenin; GastroenterologyMiceliver zonation; wnt signalling; beta catenin; hnf4Gene expressionmedicineAnimalsHumansImmunoprecipitationHepatocyteCells Culturedbeta CateninCell ProliferationMice KnockoutHepatologyAnimalReverse Transcriptase Polymerase Chain ReactionGastroenterologyWnt signaling pathwayCell DifferentiationMolecular biologyWnt Proteinsmedicine.anatomical_structureHepatocyte nuclear factor 4Hepatocyte Nuclear Factor 4Hepatocytebiology.proteinHepatocytesChromatin immunoprecipitationHumanSignal TransductionGastroenterology
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A ciliopathy complex builds distal appendages to initiate ciliogenesis

2021

ABSTRACTCells inherit two centrioles, the older of which is uniquely capable of generating a cilium. Using proteomics and super-resolved imaging, we identified a module which we term DISCO (DIStal centriole COmplex). DISCO components CEP90, MNR and OFD1 underlie human ciliopathies. This complex localized to both distal centrioles and centriolar satellites, proteinaceous granules surrounding centrioles. Cells and mice lacking CEP90 or MNR did not generate cilia, failed to assemble distal appendages, and did not transduce Hedgehog signals. Disrupting the satellite pools did not affect distal appendage assembly, indicating that it is the centriolar populations of MNR and CEP90 that are critica…

BioquímicaCentrioleGreen Fluorescent ProteinsRetinal Pigment EpitheliumBiologyCiliopathiesCell LineMice03 medical and health sciences0302 clinical medicineBacterial ProteinsGenes ReporterCiliogenesismedicineAnimalsHumansbiochemistryCiliadevelopmentHedgehogCentrioles030304 developmental biologyMice KnockoutAppendage0303 health sciencesCiliumciliaProteinsEpithelial CellscytoskeletonCell BiologyEmbryo Mammalianmedicine.diseaseCiliopathiesCell biologyMice Inbred C57BLLuminescent ProteinsCiliopathyGene Expression RegulationMicrotubule-Associated Proteins030217 neurology & neurosurgerySignal TransductionJournal of Cell Biology
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Bile acid receptor TGR5 is critically involved in preference for dietary lipids and obesity

2020

International audience; We investigated the implication of Takeda G protein-coupled receptor 5 (TGR5) in fat preference and fat sensing in taste bud cells (TBC) in C57BL/6 wild-type (WT) and TGR5 knock out (TGR5-/-) male mice maintained for 20 weeks on a high-fat diet (HFD). We also assessed the implication of TGR5 single nucleotide polymorphism (SNP) in young obese humans. The high-fat diet (HFD)-fed TGR5-/- mice were more obese, marked with higher liver weight, lipidemia and steatosis than WT obese mice. The TGR5-/- obese mice exhibited high daily food/energy intake, fat mass and inflammatory status. WT obese mice lost the preference for dietary fat, but the TGR5-/- obese mice exhibited n…

Blood GlucoseLipopolysaccharidesMale0301 basic medicine[SDV]Life Sciences [q-bio]Endocrinology Diabetes and MetabolismClinical BiochemistryBiochemistryReceptors G-Protein-CoupledMice0302 clinical medicineInsulinReceptorMice Knockout2. Zero hungerchemistry.chemical_classificationNutrition and DieteticsLipidsG protein-coupled bile acid receptor[SDV] Life Sciences [q-bio]medicine.anatomical_structuremedicine.medical_specialtyMice Transgenic030209 endocrinology & metabolismSingle-nucleotide polymorphismDiet High-FatPolymorphism Single NucleotideBile Acids and SaltsFood Preferences03 medical and health sciencesInternal medicineTaste budmedicineAnimalsObesityMolecular BiologyInflammationbusiness.industryTaste budFatty acidFatty acidmedicine.diseaseDietary FatsObesityIn vitroFatty LiverMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologychemistryFatCalciumSteatosisbusinessThe Journal of Nutritional Biochemistry
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Lipopolysaccharides-mediated increase in glucose-stimulated insulin secretion: involvement of the GLP-1 pathway.

2013

Lipopolysaccharides (LPS) of the cell wall of gram–negative bacteria trigger inflammation, which is associated with marked changes in glucose metabolism. Hyperglycemia is frequently observed during bacterial infection and it is a marker of a poor clinical outcome in critically ill patients. The aim of the current study was to investigate the effect of an acute injection or continuous infusion of LPS on experimentally induced hyperglycemia in wild-type and genetically engineered mice. The acute injection of a single dose of LPS produced an increase in glucose disposal and glucose-stimulated insulin secretion (GSIS). Continuous infusion of LPS through mini-osmotic pumps was also associated wi…

Blood GlucoseLipopolysaccharidesendocrine systemmedicine.medical_specialtyEndocrinology Diabetes and MetabolismInflammationBiologyCarbohydrate metabolismGlucagon-Like Peptide-1 ReceptorMiceGlucagon-Like Peptide 1Internal medicinePhospholipid transfer proteinInternal MedicinemedicineHyperinsulinemiaReceptors GlucagonAnimalsInsulinSecretionPhospholipid Transfer ProteinsReceptorMice Knockoutmedicine.disease3. Good healthEndocrinologyGlucoseKnockout mousemedicine.symptomAntagonismhormones hormone substitutes and hormone antagonistsDiabetes
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Temporal and tissue-specific requirements for T-lymphocyte IL-6 signalling in obesity-associated inflammation and insulin resistance

2017

Low-grade inflammation links obesity to insulin resistance through the activation of tissue-infiltrating immune cells. Interleukin-6 (IL-6) is a crucial regulator of T cells and is increased in obesity. Here we report that classical IL-6 signalling in T cells promotes inflammation and insulin resistance during the first 8 weeks on a high-fat diet (HFD), but becomes dispensable at later stages (after 16 weeks). Mice with T cell-specific deficiency of IL-6 receptor-α (IL-6RαT-KO) exposed to a HFD display improved glucose tolerance, insulin sensitivity and inflammation in liver and EWAT after 8 weeks. However, after 16 weeks, insulin resistance in IL-6RαT-KO epididymal white adipose tissue (EW…

Blood GlucoseMale0301 basic medicinemedicine.medical_specialtyTime FactorsT-LymphocytesT cellScienceGeneral Physics and AstronomyInflammationWhite adipose tissueBiologyDiet High-FatArticleGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciences0302 clinical medicineInsulin resistanceImmune systemInternal medicinemedicineAnimalsHomeostasisObesityReceptorInflammationMice KnockoutMultidisciplinaryInterleukin-6QGeneral ChemistryT lymphocyteLipid Metabolismmedicine.diseaseReceptors Interleukin-6030104 developmental biologymedicine.anatomical_structureEndocrinology030220 oncology & carcinogenesisInsulin Resistancemedicine.symptomHomeostasisSignal TransductionNature Communications
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