Search results for "U937 Cell"

showing 10 items of 34 documents

Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells

2010

MOZ and MLL, encoding a histone acetyltransferase (HAT) and a histone methyltransferase, respectively, are targets for recurrent chromosomal translocations found in acute myeloblastic or lymphoblastic leukemia. In MOZ (MOnocytic leukemia Zinc-finger protein)/CBP- or mixed lineage leukemia (MLL)-rearranged leukemias, abnormal levels of HOX transcription factors have been found to be critical for leukemogenesis. We show that MOZ and MLL cooperate to regulate these key genes in human cord blood CD34+ cells. These chromatin-modifying enzymes interact, colocalize and functionally cooperate, and both are recruited to multiple HOX promoters. We also found that WDR5, an adaptor protein essential fo…

Cancer ResearchAntigens CD34HistonesHistone H3hemic and lymphatic diseasesHistone methylationGeneticsHumansWDR5Tissue DistributionPromoter Regions GeneticHox geneneoplasmsMolecular BiologyCells CulturedHistone AcetyltransferasesHomeodomain ProteinsGeneticsBlood CellsbiologyIntracellular Signaling Peptides and ProteinsHistone-Lysine N-MethyltransferaseReceptor Cross-TalkU937 CellsHistone acetyltransferaseFetal BloodHematopoiesisCell biologyGene Expression RegulationHistone methyltransferasebiology.proteinMyeloid-Lymphoid Leukemia ProteinH3K4me3K562 CellsMyeloid-Lymphoid Leukemia ProteinProtein BindingOncogene
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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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P089 IFNγ-macrophages could mediate EMT in Crohn’s disease

2021

Abstract Background Macrophages contribute to fibrosis by releasing different mediators and the pattern of secretion may vary depending on the surrounding environment. We previously described that the mRNA expression of IFNγ was significantly higher in intestinal samples from CD patients. The aim of the present study is to analyze the role of IFNγ-treated macrophages in epithelial mesenchymal transition (EMT). Methods The mRNA and protein expression of IFN in surgical resections from Crohn′s disease. U937 were differentiated to macrophages and then treated with IFNγ (2 ng/ml) for 4 days, the mRNA expression of macrophages markers were determined by RT-PCR. IFNγ-U937 were coculture with HT29…

Crohn's diseaseU937 cellbiologybusiness.industryGastroenterologyVimentinGeneral Medicinemedicine.diseasePhenotypeEpitheliumHT29 Cellsmedicine.anatomical_structureFibrosismedicineCancer researchbiology.proteinCoculture TechniquebusinessJournal of Crohn's and Colitis
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P017 C86/CD16 macrophages accumulate in the mucosa of B3 patients and could mediate EMT in Crohn’s disease

2020

Abstract Background Macrophages contribute to fibrosis through the release of different mediators and the pattern of secretion may vary according to their phenotype. Methods The aim of the present study is to analyse the pattern of expression of macrophages, of EMT-related genes and cytokines in surgical resections from Crohn’s disease (CD, n = 43) patients which were categorised according to Montreal classification (B2 or B3); unaffected mucosa of patients with ileocecal cancer was used as control (n = 20). mRNA was isolated from intestinal samples and the expression of macrophage, EMT markers and cytokines were analysed by RT-PCR. PBMCS were isolated from healthy donors and treated during…

Crohn's diseasebiologyU937 cellbusiness.industrymedicine.medical_treatmentGastroenterologyCancerMucous membraneVimentinGeneral Medicinemedicine.diseaseCytokinemedicine.anatomical_structureFibrosismedicinebiology.proteinCancer researchbusinessInterleukin 4Journal of Crohn's and Colitis
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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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