Search results for "U937 Cells"

showing 10 items of 31 documents

In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C.

2003

In BCR-ABL-positive cells, the transcription factor STAT-5 is constitutively activated by tyrosine phosphorylation. STAT-5 activation results in upregulation of bcl-X(L) and increased resistance to induction of apoptosis. Here, we investigated the effects of imatinib mesylate and cytosine arabinoside (Ara-C) on STAT-5 tyrosine-phosphorylation, cellular proliferation and induction of apoptosis in cell lines and primary hematopoietic cells. Imatinib mesylate treatment strongly suppressed STAT-5 tyrosine-phosphorylation in K562 and primary CML blasts. In contrast to JAK-2 and PI-3-kinase inhibition, exposure of K562 cells to imatinib mesylate resulted in obvious suppression of proliferation. R…

Cancer ResearchProgrammed cell deathBlotting WesternFusion Proteins bcr-ablDown-RegulationAntineoplastic AgentsApoptosisBiologyPiperazineschemistry.chemical_compoundDownregulation and upregulationhemic and lymphatic diseasesLeukemia Myelogenous Chronic BCR-ABL PositivemedicineIn Situ Nick-End LabelingSTAT5 Transcription FactorHumansEnzyme InhibitorsPhosphorylationCell growthCytarabineImatinibTyrosine phosphorylationDrug SynergismHematologyDNAU937 CellsProtein-Tyrosine KinasesMilk ProteinsPrecipitin TestsDNA-Binding ProteinsImatinib mesylatePyrimidinesOncologychemistryApoptosisCaspasesBenzamidesCancer researchImatinib MesylateTrans-ActivatorsTyrosinePoly(ADP-ribose) PolymerasesK562 CellsCell Divisionmedicine.drugK562 cellsSignal TransductionLeukemia
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U937 variant cells as a model of apoptosis without cell disintegration

2012

AbstractThe variant cell line U937V was originally identified by a higher sensitivity to the cytocidal action of tumor necrosis factor alpha (TNFα) than that of its reference cell line, U937. We noticed that a typical morphological feature of dying U937V cells was the lack of cellular disintegration, which contrasts to the formation of apoptotic bodies seen with dying U937 cells. We found that both TNFα, which induces the extrinsic apoptotic pathway, and etoposide (VP-16), which induces the intrinsic apoptotic pathway, stimulated U937V cell death without cell disintegration. In spite of the distinct morphological differences between the U937 and U937V cells, the basic molecular events of ap…

Cell typeProgrammed cell deathBlotting WesternCellApoptosisU937 cellsDNA FragmentationBiologyModels BiologicalBiochemistrymedicineHumansCell ShapeMolecular BiologyU937 cellCytochrome cCytochromes chemic and immune systemsCell BiologyApoptotic bodyCaspase 9MitochondriaCell biologyEnzyme Activationmedicine.anatomical_structureApoptosisCell culturebiology.proteinApoptotic bodiesLymphoma Large B-Cell DiffuseCell disintegrationSignal TransductionResearch ArticleCellular and Molecular Biology Letters
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Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4

2012

Ingestion of wheat, barley, or rye triggers small intestinal inflammation in patients with celiac disease. Specifically, the storage proteins of these cereals (gluten) elicit an adaptive Th1-mediated immune response in individuals carrying HLA-DQ2 or HLA-DQ8 as major genetic predisposition. This well-defined role of adaptive immunity contrasts with an ill-defined component of innate immunity in celiac disease. We identify the α-amylase/trypsin inhibitors (ATIs) CM3 and 0.19, pest resistance molecules in wheat, as strong activators of innate immune responses in monocytes, macrophages, and dendritic cells. ATIs engage the TLR4–MD2–CD14 complex and lead to up-regulation of maturation markers a…

GliadinMice0302 clinical medicineHEK293 CellImmunology and AllergyTriticumPlant Proteins2. Zero hungerMice Knockout0303 health sciencesToll-like receptorMice Inbred C3Hfood and beveragesPlant ProteinU937 CellsAcquired immune system3. Good health030211 gastroenterology & hepatologymedicine.symptomTrypsin InhibitorsHumanSignal TransductionImmunologyMolecular Sequence DataInflammationBiologyProinflammatory cytokineCell Line03 medical and health sciencesImmune systemImmunitymedicineAnimalsHumansAmino Acid Sequence030304 developmental biologyInnate immune systemSequence Homology Amino AcidAnimalBIO/13 - BIOLOGIA APPLICATAnutritional and metabolic diseasesHordeumImmunity InnateToll-Like Receptor 4Mice Inbred C57BLCeliac DiseaseHEK293 CellsImmunologyMyeloid Differentiation Factor 88TLR4Trypsin Inhibitor
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Effects of caspase inhibitors (z-VAD-fmk, z-VDVAD-fmk) on Nile Red fluorescence pattern in 7-ketocholesterol-treated cells: Investigation by flow cyt…

2007

Background: The 7-ketocholesterol (7KC)-induced cell death has some characteristics of apoptosis and is associated with polar lipid accumulation. So, we investigated the effects of the broad-spectrum caspase inhibitor z-VAD-fmk and of the caspase-2 inhibitor z-VDVAD-fmk on lipid profile evaluated by staining with Nile Red (NR). Methods: The 7KC-treated human monocytic U937 cells were cultured in the absence or in the presence of the caspase inhibitors z-VAD-fmk or z-VDVAD-fmk. When staining with NR is performed, neutral and polar lipids have yellow and orange/red emission, respectively, and fluorescence was then analyzed by flow cytometry (FCM) and by confocal laser scanning microscopy (CLS…

HistologyConfocalCaspase 2FluorescencePathology and Forensic Medicinelaw.inventionFlow cytometryAmino Acid Chloromethyl Ketones03 medical and health scienceschemistry.chemical_compound0302 clinical medicineConfocal microscopylawOxazinesmedicineImage Processing Computer-AssistedHumans[ SDV.IB ] Life Sciences [q-bio]/BioengineeringEnzyme InhibitorsKetocholesterols030304 developmental biology[SDV.IB] Life Sciences [q-bio]/BioengineeringCell Nucleus0303 health sciencesMicroscopyMicroscopy Confocalbiologymedicine.diagnostic_testNile redLipid metabolismCell BiologyU937 CellsFlow CytometryLipid MetabolismFluorescenceMolecular biologyCaspase Inhibitors3. Good healthStainingchemistry030220 oncology & carcinogenesisbiology.protein[SDV.IB]Life Sciences [q-bio]/Bioengineeringbiological phenomena cell phenomena and immunityFactor Analysis Statistical
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Modulation of acute and chronic inflammatory processes by cacospongionolide B, a novel inhibitor of human synovial phospholipase A2.

1999

1. Cacospongionolide B is a novel marine metabolite isolated from the sponge Fasciospongia cavernosa. In in vitro studies, this compound inhibited phospholipase A2 (PLA2), showing selectivity for secretory PLA2 (sPLA2) versus cytosolic PLA2 (cPLA2), and its potency on the human synovial enzyme (group II) was similar to that of manoalide. 2. This activity was confirmed in vivo in the 8 h zymosan-injected rat air pouch, on the secretory enzyme accumulating in the pouch exudate. Cacospongionolide B, that is bioavailable when is given orally, reduced the elevated levels of sPLA2 present in paw homogenates of rats with adjuvant arthritis. 3. This marine metabolite showed topical anti-inflammator…

InflammationMaleDose-Response Relationship DrugEarU937 CellsArthritis ExperimentalPhospholipases AEnzymesRatsMicePhospholipases A24-ButyrolactoneAnti-Infective AgentsAcute DiseaseChronic DiseaseSynovial FluidPapersLeukocytesAnimalsEdemaHumansFemaleRats WistarPyransBritish journal of pharmacology
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Docosahexaenoic Acid Induces Increases in [Ca2+]ivia Inositol 1,4,5-Triphosphate Production and Activates Protein Kinase Cγ and -δ via Phosphatidylse…

2007

We investigated, in monocytic leukemia U937 cells, the effects of docosahexaenoic acid (DHA; 22:6 n-3) on calcium signaling and determined the implication of phospholipase C (PLC) and protein kinase C (PKC) in this pathway. DHA induced dose-dependent increases in [Ca2+]i, which were contributed by intracellular pool, via the production of inositol-1,4,5-triphosphate (IP3) and store-operated Ca2+ (SOC) influx, via opening of Ca2+ release-activated Ca2+ (CRAC) channels. Chemical inhibition of PLC, PKCgamma, and PKCdelta, but not of PKCbeta I/II, PKCalpha, or PKCbetaI, significantly diminished DHA-induced increases in [Ca2+]i. In vitro PKC assays revealed that DHA induced a approximately 2-fol…

Intracellular FluidDocosahexaenoic AcidsApoptosisInositol 145-TrisphosphatePhosphatidylserinesBiologyEnzyme activatorchemistry.chemical_compoundHumansCalcium SignalingPhosphatidylserine bindingProtein Kinase CProtein kinase CCalcium signalingPharmacologyBinding SitesPhospholipase CU937 CellsPhosphatidylserineMolecular biologyCell biologyEnzyme ActivationProtein Kinase C-deltachemistryDocosahexaenoic acidApoptosisMolecular Medicinelipids (amino acids peptides and proteins)Molecular Pharmacology
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Quaking and miR-155 interactions in inflammation and leukemogenesis.

2015

Quaking (QKI) is a tumor-suppressor gene encoding a conserved RNA-binding protein, whose expression is downregulated in several solid tumors. Here we report that QKI plays an important role in the immune response and suppression of leukemogenesis. We show that the expression of Qki is reduced in lipopolysaccharide (LPS)-challenged macrophages, suggesting that Qki is a key regulator of LPS signaling pathway. Furthermore, LPS-induced downregulation of Qki expression is miR-155-dependent. Qki overexpression impairs LPS-induced phosphorylation of JNK and particularly p38 MAPKs, in addition to increasing the production of anti-inflammatory cytokine IL-10. In contrast, Qki ablation decreases Fas …

LipopolysaccharidesTime Factorsmedicine.medical_treatmentmedicine.disease_causeTransgenicMiceInnatePhosphorylationChronicB-LymphocytesLeukemiaRNA-Binding ProteinsU937 CellsLymphocyticCell biologyCytokineOncologyPhosphorylationCytokinesCLL; Glioblastoma; Inflammation; MiR-155; QKI; Animals; Apoptosis Regulatory Proteins; B-Lymphocytes; Case-Control Studies; Cytokines; Humans; Immunity Innate; Inflammation; Leukemia Lymphocytic Chronic B-Cell; Lipopolysaccharides; Macrophages; Mice; Mice Transgenic; MicroRNAs; Mitogen-Activated Protein Kinases; Phosphorylation; RAW 264.7 Cells; RNA-Binding Proteins; Signal Transduction; Time Factors; Transfection; U937 Cells; OncologySignal transductionMitogen-Activated Protein KinasesSignal Transductionp38 mitogen-activated protein kinasesOncology and CarcinogenesisMice TransgenicTransfectionNOmiR-155miR-155Downregulation and upregulationmicroRNAmedicineAnimalsHumansInflammationQKIbusiness.industryMacrophagesB-CellImmunityglioblastomaLeukemia Lymphocytic Chronic B-CellImmunity InnateMicroRNAsRAW 264.7 CellsCase-Control StudiesImmunologyCarcinogenesisbusinessApoptosis Regulatory ProteinsCLLPriority Research Paper
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Inhibition of c-MYC with involvement of ERK/JNK/MAPK and AKT pathways as a novel mechanism for shikonin and its derivatives in killing leukemia cells

2015

Leukemia remains life-threatening despite remarkable advances in chemotherapy. The poor prognosis and drug resistance are challenging treatment. Novel drugs are urgently needed. Shikonin, a natural naphthoquinone, has been previously shown by us to be particularly effective towards various leukemia cell lines compared to solid tumors. However, the underlying mechanisms are still poorly understood. Here, we investigated shikonin and 14 derivatives on U937 leukemia cells. Four derivatives (isobutyrylshikonin, 2-methylbutyrylshikonin, isovalerylshikonin and β,β-dimethylacrylshikonin) were more active than shikonin. AnnexinV-PI analysis revealed that shikonins induced apoptosis. Cell cycle G1/S…

MAPK/ERK pathwayMAP Kinase Signaling Systemshikonin and its derivativesJurkat cellsProto-Oncogene Proteins c-mycCell Line TumormedicineHumansacute leukemiaExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathwayMitogen-Activated Protein Kinase KinasesLeukemiaU937 cellERK/JNK/MAP kinasesbusiness.industryAnti-Inflammatory Agents Non-SteroidalJNK Mitogen-Activated Protein KinasesU937 CellsCell cyclemedicine.diseaseLeukemiac-MYCAKT pathwayOncologyCancer researchSignal transductionbusinessProto-Oncogene Proteins c-aktResearch PaperNaphthoquinonesSignal TransductionOncotarget
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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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Defective nuclear localization of Hsp70 is associated with dyserythropoiesis and GATA-1 cleavage in myelodysplastic syndromes.

2012

Abstract Normal human erythroid cell maturation requests the transcription factor GATA-1 and a transient activation of caspase-3, with GATA-1 being protected from caspase-3–mediated cleavage by interaction with the chaperone heat shock protein 70 (Hsp70) in the nucleus. Erythroid cell dysplasia observed in early myelodysplastic syndromes (MDS) involves impairment of differentiation and excess of apoptosis with a burst of caspase activation. Analysis of gene expression in MDS erythroblasts obtained by ex vivo cultures demonstrates the down-regulation of a set of GATA-1 transcriptional target genes, including GYPA that encodes glycophorin A (GPA), and the up-regulation of members of the HSP70…

MaleErythroblasts[SDV]Life Sciences [q-bio]Biochemistry0302 clinical medicineTranscription (biology)hemic and lymphatic diseasesGene expressionErythropoiesisGATA1 Transcription FactorCells CulturedCaspaseComputingMilieux_MISCELLANEOUSOligonucleotide Array Sequence AnalysisAged 80 and over0303 health sciencesbiologyCaspase 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationU937 CellsHematologyMiddle Agedmedicine.anatomical_structure030220 oncology & carcinogenesisFemaleAdultGreen Fluorescent ProteinsImmunoblottingImmunology03 medical and health sciencesErythroid CellsmedicineHumansHSP70 Heat-Shock ProteinsTranscription factorAged030304 developmental biologyCell NucleusGene Expression ProfilingCell BiologyMolecular biologyCell nucleusMicroscopy FluorescenceApoptosisMyelodysplastic SyndromesChaperone (protein)Mutationbiology.proteinNuclear localization sequence
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