Search results for "Macrophages"

showing 10 items of 533 documents

Resveratrol: preventing properties against vascular alterations and ageing.

2005

International audience; Cardiovascular diseases are the leading cause of death in developed countries where the common pathological substrate underlying this process is atherosclerosis. Several new concepts have emerged in relation to mechanisms that contribute to the regulation of the vascular diseases and associated inflammatory effects. Recently, potential antioxidants (vitamin E, polyphenols) have received much attention as potential anti-atherosclerotic agents. Among the polyphenols with health benefic properties, resveratrol, a phytoalexin of grape, seem to be a good candidate protecting the vascular walls from oxidation, inflammation, platelet aggregation, and thrombus formation. In …

MESH : Oxidative StressAgingAntioxidantPlatelet AggregationArteriosclerosismedicine.medical_treatmentResveratrolPharmacologymedicine.disease_causeMuscle Smooth Vascularchemistry.chemical_compoundMESH : VasodilationMESH : Foam CellsMESH : Platelet AggregationStilbenesMESH : Cardiovascular DiseasesMESH : Macrophageschemistry.chemical_classificationNeovascularization PathologicPhytoalexinfood and beveragesVasodilationBiochemistryCardiovascular Diseasesmedicine.symptomBiotechnologyLipoproteinsInflammationHealth PromotionMESH : LipoproteinsBiologyMESH : StilbenesMESH : ArteriosclerosismedicineHumans[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyReactive oxygen speciesMechanism (biology)MacrophagesMESH : HumansMESH : Neovascularization PathologicMESH : Muscle Smooth VascularMESH : AgingOxidative StresschemistryAgeingResveratrolMESH : Health PromotionOxidative stressFood ScienceFoam Cells
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Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

2008

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no signifi…

MESH: InflammationGlycosylphosphatidylinositolsNeutrophilsmedicine.medical_treatmentInterleukin-1betasourisMESH: NeutrophilsMESH: VirulenceMESH: Mice KnockoutMiceMESH: Interleukin-1betaNull cellMESH: AnimalsCandida albicansPeritoneal CavityCells CulturedMice Knockout0303 health sciencesToll-like receptorbiologyVirulenceMESH: Toll-Like Receptor 2MESH: Peritoneal CavityMESH: Toll-Like Receptor 4MESH: GlycosylphosphatidylinositolsInfectious DiseasesCytokineMESH: Survival AnalysisTumor necrosis factor alphaMESH: Fungal Proteinsprotéine de la paroi cellulaireMESH: Macrophages PeritonealMESH: Cells CulturedVirulence FactorsImmunologyMicrobiologyMicrobiologyProinflammatory cytokineFungal Proteins03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsMESH: Mice030304 developmental biologyMESH: Virulence FactorsInflammation030306 microbiologyInterleukin-6Tumor Necrosis Factor-alphaMESH: Candida albicans[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologybiology.organism_classificationSurvival AnalysispathogénicitéMESH: Interleukin-6Toll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4TLR2GlycosylphosphatidylinositolMESH: Gene DeletionMESH: Tumor Necrosis Factor-alphaTLR4Macrophages Peritonealcandida albicansimmunitéGene Deletion
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Human OX40 tunes the function of regulatory T cells in tumor and nontumor areas of hepatitis C virus-infected liver tissue.

2014

International audience; Regulatory T cells (Tregs) can be considered as a mixed population of distinct subsets, endowed with a diverse extent and quality of adaptation to microenvironmental signals. Here, we uncovered an opposite distribution of Treg expansion, phenotype, and plasticity in different microenvironments in the same organ (liver) derived from patients with chronic hepatitis C: On the one side, cirrhotic and tumor fragments were moderately and highly infiltrated by Tregs, respectively, expressing OX40 and a T-bet high IFN-c – " T-helper (Th)1-suppressing " phenotype; on the other side, noncirrhotic liver specimens contained low frequencies of Tregs that expressed low levels of O…

MESH: Receptors OX40/metabolism*MESH: Interleukin-12/metabolismLiver CirrhosisMaleMacrophagemedicine.disease_causeMESH: Carcinoma Hepatocellular/immunology*T-Lymphocytes RegulatoryMESH: OX40 Ligand/metabolism0302 clinical medicineMESH: Aged 80 and overMESH: T-Lymphocytes Regulatory/physiology*MESH: Up-RegulationOX40MESH: AgedAged 80 and over0303 health scienceseducation.field_of_studyT REGMESH: Middle AgedMedicine (all)MESH: Liver Cirrhosis/immunology*Liver Neoplasmshemic and immune systemsMiddle AgedMESH: Liver Neoplasms/immunology*PhenotypeHepatitis CInterleukin-123. Good healthUp-RegulationPhenotypeLiver Neoplasm[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyInterleukin 12[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemalemedicine.symptomMESH: Hepatitis C/immunology*OX40; T REG; HEPATITIS C VIRUSHumanmedicine.medical_specialtyCarcinoma HepatocellularHepatitis C virusLiver CirrhosiPopulationInflammationchemical and pharmacologic phenomena[SDV.CAN]Life Sciences [q-bio]/CancerOX40 LigandBiologyMESH: PhenotypeMESH: Liver Neoplasms/virology03 medical and health sciencesIkaros Transcription FactorDownregulation and upregulationInternal medicinemedicineHumansMESH: Macrophages/metabolismeducation030304 developmental biologyAgedMESH: HumansHepatologyMacrophagesHEPATITIS C VIRUSMESH: Carcinoma Hepatocellular/virologyHepatologyReceptors OX40MESH: Ikaros Transcription Factor/metabolismMESH: Hepatitis C/complicationsMESH: MaleOX40 ligandImmunologyMESH: Liver Cirrhosis/virologyMESH: Female030215 immunology
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A role for miR-142-3p in colony-stimulating factor 1-induced monocyte differentiation into macrophages

2013

AbstractThe differentiation of human peripheral blood monocytes into macrophages can be reproduced ex vivo by culturing the cells in the presence of colony-stimulating factor 1 (CSF1). Using microarray profiling to explore the role of microRNAs (miRNAs), we identified a dramatic decrease in the expression of the hematopoietic specific miR-142-3p. Up- and down-regulation of this miRNA in primary human monocytes altered CSF1-induced differentiation of monocytes, as demonstrated by changes in the expression of the cell surface markers CD16 and CD163. One of the genes whose expression is repressed by miR-142-3p encodes the transcription factor Early Growth Response 2 (Egr2). In turn, Egr2 assoc…

Macrophage colony-stimulating factorAntigens Differentiation MyelomonocyticDown-RegulationChronic myelomonocytic leukemiaReceptors Cell SurfaceCD16BiologyGPI-Linked ProteinsMonocyte–macrophage differentiationMonocytesChronic myelomonocytic leukemiaAntigens CDCell Line TumorMiR-142-3pmedicineHumansTranscription factorMolecular BiologyEarly Growth Response Protein 2Early Growth Response Protein 1Cluster of differentiationMolecular circuitryMacrophage Colony-Stimulating FactorMacrophagesReceptors IgGCell DifferentiationLeukemia Myelomonocytic ChronicCell Biologymedicine.diseaseUp-RegulationRepressor ProteinsMicroRNAsHaematopoiesisMonocyte differentiationCancer researchEgr2K562 CellsK562 cellsBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Caspase-8 prevents sustained activation of NF-kappaB in monocytes undergoing macrophagic differentiation.

2006

Abstract Caspases have demonstrated several nonapoptotic functions including a role in the differentiation of specific cell types. Here, we show that caspase-8 is the upstream enzyme in the proteolytic caspase cascade whose activation is required for the differentiation of peripheral-blood monocytes into macrophages. On macrophage colony-stimulating factor (M-CSF) exposure, caspase-8 associates with the adaptor protein Fas-associated death domain (FADD), the serine/threonine kinase receptor-interacting protein 1 (RIP1) and the long isoform of FLICE-inhibitory protein FLIP. Overexpression of FADD accelerates the differentiation process that does not involve any death receptor. Active caspase…

Macrophage colony-stimulating factorCellular differentiationFas-Associated Death Domain ProteinImmunologyCaspase 8BiochemistryMonocytesArticle03 medical and health sciences0302 clinical medicineCell Line TumormedicineHumansFADDCaspase030304 developmental biologyDeath domain0303 health sciencesCaspase 8biologyMonocyteMacrophage Colony-Stimulating FactorMacrophagesNF-kappa BSignal transducing adaptor proteinRNA-Binding ProteinsCell DifferentiationCell BiologyHematologyMolecular biologyNuclear Pore Complex Proteinsmedicine.anatomical_structure030220 oncology & carcinogenesisbiology.proteinBlood
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Colony-stimulating factor-1-induced oscillations in phosphatidylinositol-3 kinase/AKT are required for caspase activation in monocytes undergoing dif…

2009

Abstract The differentiation of human peripheral blood monocytes into resident macrophages is driven by colony-stimulating factor-1 (CSF-1), which upon interaction with CSF-1 receptor (CSF-1R) induces within minutes the phosphorylation of its cytoplasmic tyrosine residues and the activation of multiple signaling complexes. Caspase-8 and -3 are activated at day 2 to 3 and contribute to macrophage differentiation, for example, through cleavage of nucleophosmin. Here, we show that the phosphatidylinositol-3 kinase and the downstream serine/threonine kinase AKT connect CSF-1R activation to caspase-8 cleavage. Most importantly, we demonstrate that successive waves of AKT activation with increasi…

Macrophage colony-stimulating factorCellular differentiationImmunologyImmunoblottingApoptosisBiologyBiochemistryMonocytesImmunoenzyme TechniquesPhosphatidylinositol 3-KinasesHumansImmunoprecipitationRNA MessengerPhosphorylationProtein kinase BCells CulturedPhosphoinositide-3 Kinase InhibitorsMitogen-Activated Protein Kinase 1Caspase 8Mitogen-Activated Protein Kinase 3MAP kinase kinase kinaseKinaseAkt/PKB signaling pathwayReverse Transcriptase Polymerase Chain ReactionMacrophage Colony-Stimulating FactorMacrophagesCell DifferentiationCell BiologyHematologyFlow CytometryCell biologyEnzyme ActivationPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionBlood
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Fine-tuning nucleophosmin in macrophage differentiation and activation

2011

Abstract M-CSF–driven differentiation of peripheral blood monocytes is one of the sources of tissue macrophages. In humans and mice, the differentiation process involves the activation of caspases that cleave a limited number of proteins. One of these proteins is nucleophosmin (NPM1), a multifunctional and ubiquitous protein. Here, we show that caspases activated in monocytes exposed to M-CSF cleave NPM1 at D213 to generate a 30-kDa N-terminal fragment. The protein is further cleaved into a 20-kDa fragment, which involves cathepsin B. NPM1 fragments contribute to the limited motility, migration, and phagocytosis capabilities of resting macrophages. Their activation with lipopolysaccharides …

Macrophage colony-stimulating factorLipopolysaccharidesCellular differentiationImmunologyBiochemistryProinflammatory cytokine03 medical and health sciencesPhagocytes Granulocytes and MyelopoiesisMice0302 clinical medicineAnimalsHumansNuclear proteinCaspaseCells Cultured030304 developmental biologyMice Knockout0303 health sciencesNucleophosminbiologyMacrophage Colony-Stimulating FactorMacrophagesNuclear ProteinsCell DifferentiationCell BiologyHematologyMacrophage ActivationNFKB1Molecular biologyCathepsinsCell biologyProtein Structure TertiaryCXCL1Mice Inbred C57BL030220 oncology & carcinogenesisCaspasesbiology.proteinNucleophosminProtein Processing Post-TranslationalBlood
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CSF-1 signals directly to renal tubular epithelial cells to mediate repair in mice

2009

金沢大学医薬保健研究域医学系

Macrophage colony-stimulating factorPathologymedicine.medical_specialtymedicine.medical_treatmenteducation030232 urology & nephrologyApoptosisReceptor Macrophage Colony-Stimulating FactorBiology03 medical and health sciencesParacrine signallingMice0302 clinical medicineFibrosismedicineAnimalsHumansRegenerationAutocrine signalling030304 developmental biologyCell Proliferation0303 health sciencesMice Inbred C3HGrowth factorMacrophage Colony-Stimulating FactorMacrophageshemic and immune systemsEpithelial CellsGeneral Medicinemedicine.diseaseFibrosis3. Good healthKidney TubulesIntegrin alpha MApoptosisReperfusion Injurybiology.proteinCancer researchReperfusion injurytissuesResearch Article
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Alpha-defensins secreted by dysplastic granulocytes inhibit the differentiation of monocytes in chronic myelomonocytic leukemia.

2010

Abstract Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic disorder that occurs in elderly patients. One of the main diagnostic criteria is the accumulation of heterogeneous monocytes in the peripheral blood. We further explored this cellular heterogeneity and observed that part of the leukemic clone in the peripheral blood was made of immature dysplastic granulocytes with a CD14−/CD24+ phenotype. The proteome profile of these cells is dramatically distinct from that of CD14+/CD24− monocytes from CMML patients or healthy donors. More specifically, CD14−/CD24+ CMML cells synthesize and secrete large amounts of alpha-defensin 1-3 (HNP1-3). Recombinant HNPs inhibit macrophage co…

Macrophage colony-stimulating factoralpha-DefensinsCD14Cellular differentiationImmunologyLipopolysaccharide ReceptorsChronic myelomonocytic leukemiaUridine TriphosphateBiologyGranulocyteBiochemistryMonocytesUridine DiphosphatemedicineMacrophageHumansReceptors Purinergic P2MonocyteMacrophage Colony-Stimulating FactorMacrophagesCD24 AntigenCell DifferentiationLeukemia Myelomonocytic ChronicCell BiologyHematologymedicine.diseaseHaematopoiesismedicine.anatomical_structureCancer researchCytokinesGranulocytesBlood
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Phytochemical indicaxanthin prevents 7-ketocholesterol-induced oxidative stress and cell cycle arrest in murine macrophages

2011

MacrophagesApoptosiIndicaxanthin7-Ketocholesterol
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