Search results for "Flow Cytometry"

showing 10 items of 814 documents

CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor-beta-dependent manner.

2007

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, redu…

MESH : CytokinesMESH: Flow CytometryMESH : Immunity NaturalMESH: T-LyLymphocyte ActivationT-Lymphocytes RegulatoryMiceInterleukin 210302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betaNeoplasmsMESH : Receptors ImmunologicMESH : Cell ProliferationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH: NeoplasmsIL-2 receptorReceptors Immunologic0303 health sciencesMESH: Cytokineshemic and immune systemsFlow CytometryNatural killer T cell3. Good healthCell biologyKiller Cells Naturalmedicine.anatomical_structureNK Cell Lectin-Like Receptor Subfamily KInterleukin 12CytokinesReceptors Natural Killer Cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyFranceMESH : Killer Cells NaturalMESH : Cytotoxicity Tests ImmunologicMESH: Killer Cells NaturalMESH: Cell Line TumorMESH : Flow CytometryImmunologychemical and pharmacologic phenomenaMESH: Cytotoxicity Tests ImmunologicMESH : Mice Inbred C57BLBiologyArticleNatural killer cell03 medical and health sciencesMESH: Mice Inbred C57BLCell Line TumorMESH: Cell ProliferationMESH : MicemedicineAnimalsHumansAntigen-presenting cellMESH: Lymphocyte ActivationMESH : FranceMESH: MiceMESH: Receptors ImmunologicMESH : Lymphocyte ActivationCell Proliferation030304 developmental biologyMESH: Immunity NaturalLymphokine-activated killer cellMESH: HumansMESH : Cell Line TumorMESH : HumansCytotoxicity Tests ImmunologicNKG2DMESH : T-LyMESH : NeoplasmsImmunity InnateMice Inbred C57BLMESH: FranceMESH : Animals030215 immunology
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3-Deazaneplanocin A (DZNep), an Inhibitor of the Histone Methyltransferase EZH2, Induces Apoptosis and Reduces Cell Migration in Chondrosarcoma Cells

2014

Objective Growing evidences indicate that the histone methyltransferase EZH2 (enhancer of zeste homolog 2) may be an appropriate therapeutic target in some tumors. Indeed, a high expression of EZH2 is correlated with poor prognosis and metastasis in many cancers. In addition, 3-Deazaneplanocin A (DZNep), an S-adenosyl-L homocysteine hydrolase inhibitor which induces EZH2 protein depletion, leads to cell death in several cancers and tumors. The aim of this study was to determine whether an epigenetic therapy targeting EZH2 with DZNep may be also efficient to treat chondrosarcomas. Methods EZH2 expression was determined by immunohistochemistry and western-blot. Chondrosarcoma cell line CH2879…

MESH: Cell DeathAdenosine[SDV]Life Sciences [q-bio]Cancer Treatmentlcsh:MedicineMESH: Flow CytometryApoptosischemistry.chemical_compoundSpectrum Analysis Techniques0302 clinical medicineCell MovementMolecular Cell BiologyMedicine and Health Sciences3-Deazaneplanocin AMESH: Epigenesis GeneticEnzyme Inhibitorslcsh:Science0303 health sciencesMultidisciplinaryCell DeathbiologyReverse Transcriptase Polymerase Chain ReactionEZH2Polycomb Repressive Complex 2DrugsCell migrationMESH: ChondrosarcomaFlow Cytometry3. Good healthHistone[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemOncologyConnective TissueCell ProcessesSpectrophotometry030220 oncology & carcinogenesisHistone methyltransferaseHistone MethyltransferasesMESH: 3-deazaneplanocinCytophotometryAnatomyMESH: Polycomb Repressive Complex 2Epigenetic therapyMESH: Histone methyltransferaseResearch ArticleProgrammed cell deathHistologyChondrosarcoma[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular Biologymacromolecular substancesResearch and Analysis MethodsCell GrowthEpigenetic Therapy03 medical and health sciencesRheumatologyCell Line TumorMESH: Blotting WesternHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEZH2Tumors030304 developmental biologyMESH: Apoptosislcsh:RMESH: Histone-Lysine N-MethyltransferaseBiology and Life SciencesMESH: ImmunohistochemistryHistone-Lysine N-MethyltransferaseCell BiologyBiological TissueCartilageHistone methyltransferasechemistryApoptosisbiology.proteinCancer researchMESH: EZH2 protein humanlcsh:QCytometry
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FRET multiphoton spectral imaging microscopy of 7-ketocholesterol and Nile Red in U937 monocytic cells loaded with 7-ketocholesterol.

2004

To show the effect of 7-ketocholesterol (7KC) on cellular lipid content by means of flow cytometry and the interaction of 7KC with Nile Red (NR) via ultraviolet fluorescence resonance energy transfer (FRET) excitation of NR on U937 monocytic cells by means of 2-photon excitation confocal laser scanning microscopy (CLSM).Untreated and 7KC-treated U937 cells were stained with NR and analyzed by flow cytometry and CLSM. 3D sequences of images were obtained by spectral analysis in a 2-photon excitation CLSM and analyzed by the factor analysis of medical image sequences (FAMIS) algorithm, which provides factor curves and images. Factor images are the result of the FAMIS image processing method, …

MESH: Cell DeathMESH: Fluorescence Resonance Energy TransferMESH: Mitochondria[SDV.IB.IMA]Life Sciences [q-bio]/Bioengineering/ImagingMESH : Flow CytometryMESH: Flow CytometryMESH: U937 CellsMESH: MonocytesMonocytesMembrane PotentialsMESH : Staining and LabelingMESH : Microscopy Fluorescence MultiphotonOxazinesFluorescence Resonance Energy TransferImage Processing Computer-AssistedHumansMESH: Membrane PotentialsMESH: Microscopy ConfocalMESH : Membrane PotentialsMESH : Fluorescent DyesMESH : Microscopy ConfocalKetocholesterols[ SDV.IB.IMA ] Life Sciences [q-bio]/Bioengineering/ImagingFluorescent DyesMESH : KetocholesterolsMicroscopy ConfocalMESH: HumansMESH : OxazinesCell DeathStaining and LabelingMESH : HumansMESH: KetocholesterolsU937 CellsFlow CytometryMESH: Fluorescent DyesMESH: Image Processing Computer-AssistedMitochondriaMESH: Staining and Labeling[SDV.IB.IMA] Life Sciences [q-bio]/Bioengineering/ImagingMicroscopy Fluorescence MultiphotonMESH : MonocytesMESH : Fluorescence Resonance Energy TransferMESH : Cell DeathMESH : U937 CellsMESH: Microscopy Fluorescence MultiphotonMESH : MitochondriaMESH: OxazinesMESH : Image Processing Computer-Assisted
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Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

2009

Cell death is essential for a plethora of physiological processes, and its deregulation characterizes numerous human diseases. Thus, the in-depth investigation of cell death and its mechanisms constitutes a formidable challenge for fundamental and applied biomedical research, and has tremendous implications for the development of novel therapeutic strategies. It is, therefore, of utmost importance to standardize the experimental procedures that identify dying and dead cells in cell cultures and/or in tissues, from model organisms and/or humans, in healthy and/or pathological scenarios. Thus far, dozens of methods have been proposed to quantify cell death-related parameters. However, no guid…

MESH: Cell DeathcytofluorometryMESH : Microscopy Fluorescenceved/biology.organism_classification_rank.speciesCellMESH: Flow CytometryMESH: Microscopy FluorescenceApoptosisfluorescence microscopyMESH: Eukaryotic CellsAnnexin Vnecrosis0302 clinical medicineEukaryotic Cells/cytologyMitochondrial membrane permeabilizationScanningMESH : ImmunoblottingGeneticsApoptosis; Cell Death; Eukaryotic Cells/cytology; Flow Cytometry; Guidelines as Topic; Humans; Immunoblotting; Microscopy Electron Scanning; Microscopy Fluorescence; Spectrometry Fluorescence0303 health sciencesMicroscopyMESH : Spectrometry FluorescenceMESH: ImmunoblottingCell DeathMESH: Guidelines as Topic//purl.org/becyt/ford/3.1 [https]Bioquímica y Biología MolecularFlow Cytometry3. Good healthTunelMedicina Básicamedicine.anatomical_structureEukaryotic Cellscaspases030220 oncology & carcinogenesis//purl.org/becyt/ford/3 [https]MESH: Spectrometry FluorescenceMESH : Microscopy Electron ScanningProgrammed cell deathautophagyCIENCIAS MÉDICAS Y DE LA SALUDMESH: Microscopy Electron ScanningMESH : Flow CytometrycaspaseImmunoblottingGuidelines as TopicComputational biologyBiologyElectronFluorescenceArticle03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyModel organismddc:612mitotic catastropheMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Guidelines as Topic030304 developmental biologycell death; Apoptosis; caspase; autophagy; Oxidative stress; fluorescence microscopyMESH: Humansved/biologySpectrometryInterpretation (philosophy)MESH: ApoptosisMESH : Eukaryotic CellsMESH : HumansApoptosis; Eukaryotic Cells; Flow Cytometry; Guidelines as Topic; Humans; Immunoblotting; Microscopy Electron Scanning; Microscopy Fluorescence; Spectrometry Fluorescence; Cell Death; Molecular Biology; Cell Biologyimmunofluorescence microscopyCell BiologySpectrometry FluorescenceMicroscopy FluorescenceOxidative stressMESH : Cell DeathCancer cellMicroscopy Electron ScanningMESH : Apoptosis
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Toxicity of ligand-dependent Cre recombinases and generation of a conditional Cre deleter mouse allowing mosaic recombination in peripheral tissues.

2007

Ligand-activated Cre recombinases are widely used for studying gene function in vitro and in conditional mouse models. To compare ligand-dependent Cre recombinases, different Cre estrogen receptor fusions were introduced into the ROSA26 locus of embryonic stem (ES) cells and assayed for genotoxicity and recombination efficiency. Of the tested recombinases, the CreERT2 variant showed no toxicity and was highly responsive to ligand induction. To constitutively express CreERT2 in mice and also to clarify whether the CreERT2 system displays background activity, we generated a knock-in mouse line harboring the CreERT2 coding region under the control of the ROSA26 locus. Analysis of this ROSA26-…

MESH: IntegrasesPhysiologyMESH: Mice TransgenicTransgeneMice TransgenicMESH: Flow Cytometry[SDV.CAN]Life Sciences [q-bio]/CancerBiologyLigandsGreen fluorescent proteinMiceMESH: Brain[SDV.CAN] Life Sciences [q-bio]/CancerGenes ReporterGene expressionGeneticsRecombinaseMESH: LigandsAnimalsMESH: AnimalsMESH: Models GeneticGeneMESH: MiceRecombination GeneticIntegrasesModels GeneticMosaicismMESH: GenomicsMESH: Genes ReporterMESH: DNABrainDNAGenomicsFlow CytometryEmbryonic stem cellMolecular biologyPhenotypeDisease Models AnimalMESH: Gene DeletionMESH: Recombination GeneticMESH: MosaicismMESH: Disease Models AnimalFunctional genomicsGene Deletion
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Semicarbazide-sensitive amine oxidase/vascular adhesion protein-1 deficiency reduces leukocyte infiltration into adipose tissue and favors fat deposi…

2009

1525-2191 (Electronic) Journal Article; Obesity is associated with low-grade inflammation and leukocyte infiltration in white adipose tissue (WAT) and is linked to diabetic complications. Semicarbazide-sensitive amine oxidase, also known as vascular adhesion protein-1 (SSAO/VAP-1), is a membrane protein that is highly expressed in adipocytes and is also present on the endothelial cell surface where it is involved in leukocyte extravasation. We studied fat deposition and leukocyte infiltration in WAT of mice with a null mutation in the amine oxidase copper-containing-3 (AOC3) gene encoding SSAO/VAP-1. Both epididymal and inguinal WATs were larger in 6-month-old AOC3-KO males than in age-matc…

MESH: SemicarbazidesAOC3Obesity/geneticsAdipose tissueMESH: Flow CytometryWhite adipose tissueInbred C57BLMESH: Mice KnockoutTransgenicMiceLeukocytesMESH: ObesityMESH: AnimalsMice KnockoutAmine oxidase (copper-containing)food and beveragesNatural killer T cellFlow CytometryLeukocyte extravasationSemicarbazidesCell Adhesion Molecules/*deficiency/*geneticsAdipose TissueMESH: Cell Adhesion MoleculesLeukocytes/*physiologyAmine Oxidase (Copper-Containing)medicine.symptomInfiltration (medical)MESH: Adipose Tissuemedicine.medical_specialtyMESH: Mice TransgenicKnockoutMice TransgenicInflammation[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyMESH: Monoamine OxidasePathology and Forensic MedicineMESH: LeukocytesMonoamine Oxidase/*deficiencyMESH: Mice Inbred C57BLInternal medicinemedicineAnimalsHumansObesityMonoamine OxidaseMESH: Mice[SDV.BC] Life Sciences [q-bio]/Cellular BiologyMESH: HumansAmine Oxidase (Copper-Containing)/*deficiency/*geneticsmedicine.diseaseAdipose Tissue/pathology/*physiologyMice Inbred C57BLEndocrinologyImmunologyMESH: Amine Oxidase (Copper-Containing)Semicarbazides/*pharmacologyCell Adhesion MoleculesRegular Articles
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Novel combination of celecoxib and proteasome inhibitor MG132 provides synergistic antiproliferative and proapoptotic effects in human liver tumor ce…

2010

Molecular targeted therapy has shown promise as a treatment for advanced hepatocellular carcinoma (HCC). Celecoxib (Celebrex®) exhibits antitumor effects in human HCC cells, and its mechanism of action is mediated either by its ability to inhibit cyclooxygenase 2 (COX-2) or by a number of various other COX-2 independent effects. Proteasome inhibitors (PIs) can exert cell growth inhibitory and apoptotic effects in different tumor cell types, including HCC cells. The present study examined the interaction between celecoxib and the PI MG132 in two human liver tumor cell lines HepG2 and HA22T/VGH. Our data showed that each inhibitor reduced proliferation and induced apoptosis in a dose-dependen…

MG132TRB3Programmed cell deathLeupeptinsBlotting WesternApoptosisUPRPharmacologyCysteine Proteinase Inhibitorschemistry.chemical_compoundMG132medicineHumansViability assayHCCMolecular BiologyCell ProliferationSettore MED/12 - GastroenterologiaGene knockdownSulfonamidesbiologyCyclooxygenase 2 InhibitorsCell growthReverse Transcriptase Polymerase Chain ReactionDrug SynergismCell BiologyHep G2 CellsCOX-2ER stress responseFlow CytometryapoptosiproteasomechemistryApoptosisCelecoxibSettore BIO/14 - Farmacologiabiology.proteinProteasome inhibitorPyrazolesCyclooxygenaseDevelopmental Biologymedicine.drug
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Alveolar macrophage dynamics in murine lung regeneration

2012

In most mammalian species, the removal of one lung results in dramatic compensatory growth of the remaining lung. To investigate the contribution of alveolar macrophages (AMs) to murine post-pneumonectomy lung growth, we studied bronchoalveolar lavage (BAL)-derived AM on 3, 7, 14 and 21 days after left pneumonectomy. BAL demonstrated a 3.0-fold increase in AM (CD45(+), CD11b(-), CD11c(+), F4/80(+), Gr-1(-)) by 14 days after pneumonectomy. Cell cycle flow cytometry of the BAL-derived cells demonstrated an increase in S + G2 phase cells on days 3 (11.3 ± 2.7%) and 7 (12.1 ± 1.8%) after pneumonectomy. Correspondingly, AM demonstrated increased expression of VEGFR1 and MHC class II between days…

MHC class IIeducation.field_of_studyLungbiologymedicine.diagnostic_testPhysiologymedicine.medical_treatmentClinical BiochemistryPopulationCD11cCell Biologyrespiratory systemFlow cytometryAndrologyPneumonectomyBronchoalveolar lavagemedicine.anatomical_structureImmunologyAlveolar macrophagebiology.proteinmedicineeducationJournal of Cellular Physiology
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Alveolar Epithelial Dynamics in Postpneumonectomy Lung Growth

2013

The intimate anatomic and functional relationship between epithelial cells and endothelial cells within the alveolus suggests the likelihood of a coordinated response during postpneumonectomy lung growth. To define the population dynamics and potential contribution of alveolar epithelial cells to alveolar angiogenesis, we studied alveolar Type II and I cells during the 21 days after pneumonectomy. Alveolar Type II cells were defined and isolated by flow cytometry using a CD45(-) , MHC class II(+) , phosphine(+) phenotype. These phenotypically defined alveolar Type II cells demonstrated an increase in cell number after pneumonectomy; the increase in cell number preceded the increase in Type …

MHC class IIeducation.field_of_studyPathologymedicine.medical_specialtyHistologyLungmedicine.diagnostic_testbiologyCell growthAngiogenesisPopulationWild typeInflammationrespiratory systemMolecular biologyFlow cytometrymedicine.anatomical_structuremedicinebiology.proteinAnatomymedicine.symptomeducationEcology Evolution Behavior and SystematicsBiotechnologyThe Anatomical Record
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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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