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Results for “U937 Cells”

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At least 19 recordsLinked to original sources

PubMed1985

Biosynthesis of complement protein D by HepG2 cells: a comparison of D produced by HepG2 cells, U937 cells and blood monocytes.

The biosynthesis of complement protein D of the alternative pathway by HepG2 cells, a human hepatocyte cell line, was studied and compared to the biosynthesis of D by U937 cells and blood monocytes. Increasing amounts of antigenic D were detected in HepG2 cell culture supernatants by radioimmunoassay. The kinetics of D synthesis and secretion by HepG2 cells was followed in a pulse-chase study using [35S]cysteine. As analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by autoradiography, only a single D band was seen intra- and extracellularly and both forms had the same apparent molecular weight as D synthesized by U937 cells or purified from serum. Treatment of HepG2 and U937 cells with canavanine, an arginine amino acid analog, to inhibit intracellular processing resulted in slight depression of the apparent molecular weight of D synthesized by these cells. D synthesized by blood monocytes had an apparent molecular weight similar to that synthesized by HepG2 and U937 cells, suggesting that these cell lines do not synthesize and process D differently than normal monocytes. The data demonstrate that the hepatocyte is a site of D synthesis and suggest that D is not synthesized as a precursor molecule.

Canavanine↗

PubMed1991

Thrombospondin production and thrombospondin-mediated adhesion in U937 cells.

U937 cells have low levels of surface thrombospondin (TSP) under control conditions but express higher levels after treatment for 1 day with 100 nM phorbol myristate acetate (PMA). Increased surface expression is due, in part, to increased biosynthesis. Untreated U937 cells do not adhere to TSP-coated plastic culture dishes but adhere strongly to TSP after stimulation with PMA. Untreated U937 cells also adhere weakly to endothelial cell monolayers while PMA-treated U937 cells attach strongly to monolayers of rat pulmonary artery endothelial cells. Endothelial cell adhesion appears to be mediated, in part, by TSP since antibodies to TSP partially inhibit.

Animals↗

PubMed1994

Effects of interferon-alpha on a reduced release of interleukin-8 from latently HIV-1-infected monocytic cell line U937 cells.

The effects of human interferon-alpha (IFN-alpha) on the release of an antimicrobial interleukin, interleukin-8 (IL-8), from human immunodeficiency virus type 1 (HIV-1)-infected myelomonocytic cell line, U937, were studied in vitro to evaluate the potential of IFN-alpha in the management of acquired immunodeficiency syndrome (AIDS)-associated opportunistic diseases. The latently HIV-1-infected U937 cells (U937/HIV-1(L)) showed a marked reduction of IL-8 secretion as compared to uninfected U937 cells, whereas IL-8 release from productively HIV-1-infected U937 cells was comparable to uninfected cells. The IFN-alpha recovered partially the reduced IL-8 level from U937/HIV-1(L) cells in a dose-dependent manner. Any significant inhibition of IFN-alpha-augmented IL-8 secrement by anti-IL-1 antibody was not observed, suggesting that the enhanced IL-8 secretion occurred without augmenting IL-1 production. The IFN-alpha-augmented IL-8 secretion from latently HIV-1-infected U937 cells may suggest a beneficial potential of IFN-alpha in a treatment of bacterial or fungal infection frequently seen in patients with progressive stages of HIV-1 infection.

Acquired Immunodeficiency Syndrome↗

PubMed1993

Inhibitory effect of azelastine, a potent antiallergic agent, on release of tumor necrosis factor-alpha from activated human peripheral blood mononuclear cells and U937 cells.

It is generally accepted that tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine which is involved in the regulation of inflammation as well as immunity. In the present study, we investigated whether azelastine, a potent antiallergic agent, affects release of TNF-alpha from peripheral blood mononuclear cells (PBMC) and U937 cell line in vitro. When human PBMC and U937 cells were stimulated by phytohemagglutinin (PHA) and 12-0-tetradecanoyl-phorbol-13-acetate (TPA), respectively, the cells released significant amounts of TNF-alpha as determined by TNF-alpha-specific enzyme immunoassay. TNF-alpha levels in the culture supernatant of PHA-stimulated human PBMC and TPA-activated U937 cells decreased in a dose-dependent manner when these cells were cultured in the presence of azelastine. This inhibitory effect of azelastine was obtained at concentrations where the drug produced no toxicity. Moreover, azelastine also inhibited release of TNF-alpha from U937 cells which were already activated by TPA. These results suggest that the inhibitory effect of azelastine on TNF-alpha release plays an important role in its antiallergic action in addition to inhibition and/or antagonism of histamine and leukotrienes, which has been previously reported.

Depression, Chemical↗

PubMed2006

[Effect of ginkgolide B on the function of rat aorta smooth cells and U937 cells stimulated by oxLDL].

AIM: To investigate the effect of ginkgolide B on the proliferation of VSMC and the secretion of chemokines by U937 cells stimulated by oxLDL or PAF. In addition, to analyze whether the effect of oxLDL is mediated through PAF receptor. METHODS: Using 3H-Tdr incorporation assay, the proliferation of VSMC was measured. The protein and mRNA level of MCP-1 and IL-8 in U937 cells were determined by RT-PCR and ELISA. Using Western blotting the p65 and IkappaB was quantified. The binding of oxLDL to U937 cell was measured by a radio-ligand binding assay of 3H-PAF. RESULTS: Ginkgolide B inhibited, in dose-dependent manner, the proliferation of VSMC and the secretion of chemokines by U937 cells stimulated by oxLDL, and inhibited the oxLDL-induced p65 activation and depletion of IKappaB. oxLDL inhibited PAF binding to U937 cells. CONCLUSION: Ginkgolide B, as a PAF antagonist, possesses the effect of inhibiting the proliferation of VSMC and the secretion of chemokines by U937 cells stimulated by oxLDL in vitro. The effect of oxLDL is, at least in part, mediated through PAF receptor.

Animals↗

PubMed2000

[The difference of thrombin-induced TF/uPAR mRNAs expressions in cultured endothelial cells and U937 cell line].

OBJECTIVE: To compare the effects of thrombin on the expression of the tissue factor (TF) and urokinase-type plasminogen activator receptor (uPAR) mRNA in the cultured vascular endothelial cells (VEC) and U937 cell line. METHODS: Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to detect the mRNA levels of TF and uPAR genes in the cultured cells under stimulation of thrombin, inactivated thrombin (DFP-T), or at the presence of the inducers and anti-thrombin receptor antibody (ATR-Ab). RESULTS: In U937 cells, the TF and uPAR mRNA expression induced by thrombin could be fully quenched with the ATR-Ab, but in VEC, even at the presence of ATR-Ab, there still was a little stimulative effect of thrombin revealed. DFP-T had no effect on the expression of TF and uPAR mRNA in U937 cells, but could elicit a faint reaction in VEC. CONCLUSION: The induction effects on TF and uPAR mRNA expression in both of the cultured cells by thrombin were mainly dependent on the TR activation, which may not be the unique pathway for thrombin to induce TF and uPAR mRNA expression in VEC.

Cells, Cultured↗

PubMedDate not supplied

5,8,11,14-eicosatetraynoic acid-induced differentiation of U937 cells.

U937 cells, transformed human monocyte/macrophage precursors, incubated with 5,8,11,14 eicosatetraynoic acid (ETYA), a competitive in vitro and in vivo inhibitor of arachidonic acid, develop properties consistent with a form of cellular differentiation. In order to define the extent of this differentiation and decide whether a monocyte or macrophage-like cell developed, control cells and cells cultured for three days with 40 microns ETYA were examined by transmission electron microscopy. Control cells were characterized by oval nuclei, a high nuclear to cytoplasmic ratio, a cytoplasm with a relative paucity of mitochondria, vesicles and vacuoles, and a Golgi apparatus that was not extensively developed. Ribosomes and putative ribosome-like granules were frequently "grouped" in the cytoplasm, rather than as single granules or in association with the endoplasmic reticulum. The plasma membrane included a discrete region of fimbriated structures that were distinct from pseudopodia. Such structures frequently are expressed in embryonic and transformed cells and may be associated with motility, metastases, with immunologic reactions or with endocytosis. After culture with 40 microns ETYA for three or more days, a morphology consistent with that of immature monocytes developed. These characteristics included lobulated nuclei, a reversal of the nuclear to cytoplasmic ratio, an increased complexity and development of the cytoplasmic components and the disappearance of the fimbriated plasma membrane structures. In addition, "grouped" ribosomes were less evident.(ABSTRACT TRUNCATED AT 250 WORDS)

5,8,11,14-Eicosatetraynoic Acid↗

PubMed1990

Tropism of human immunodeficiency virus 1 isolates for H9 cells and U937 cells.

Human immunodeficiency virus 1 (HIV-1) produced in the human T lymphoblastoid H9 cell line infected cells of that line more readily than cells of the human monocytoid U937 line. While both cell lines expressed detectable levels of the CD4 molecule on their surfaces, the H9 and U937 cell lines differed in expression of major histocompatibility complex class I and class II antigens. Both H9 and U937 cells were infected initially with HIV-1 derived from H9 cells. Cell-free culture supernatants were harvested after the cells had been infected for at least 1 month. Culture supernatant from HIV-infected H9 cells was used to infect H9 and U937 cells. Conversely, culture supernatant from HIV-infected U937 cells was used to infect H9 and U937 cells. The percentages of cells infected at each of several time points during the first few days after infection were determined by flow cytometric analysis of cell-associated HIV-1 major core protein p24. Infection of each cell line was more efficient when the cell type infected was identical to that in which the infecting supernatant was produced. However, this difference in tropism was not generated early after infection of each cell line, as might have been expected if this effect were mediated by cell surface molecules acquired during the process of budding through the cell membrane.

Antigens, Surface↗

PubMed1997

Inhibitors of arachidonic acid metabolism reduce DNA and nuclear fragmentation induced by TNF plus cycloheximide in U937 cells.

U937 human myeloid leukemia cells are induced to apoptosis by tumour necrosis factor (TNF) plus cycloheximide (CHX). We have analysed the effect of various inhibitors of the arachidonic acid (AA) metabolism on several features of this process. The formation of high molecular weight and oligonucleosomal DNA fragments as well as nuclear fragmentation were reduced by inhibitors of 5-lipoxygenase (BWA4C and BWB70C), 5-LO activating protein (MK-886), and cytosolic PLA2 (AACOCF3). None of these agents blocked the morphological changes detected by microscopy or flow cytometry, phosphatidylserine exposure on the cell surface or Caspase 3-like activation. AA also induced nuclear fragmentation at a concentration of 1-20 microM. However, the mechanisms by which these inhibitors act, remain unexplained since there was no 5-LO expression in the U937 cells and no AA release followed their stimulation with TNF plus CHX.

Journal Article↗

PubMed1983

Vitamin D metabolites change the phenotype of monoblastic U937 cells.

U937 is a human-derived lymphoma cell line that has monoblastic properties and high-affinity receptors for 1 alpha,-dihydroxyvitamin D3. Incubation of these cells with the vitamin D metabolite at 10 nM for 5 days produced marked stimulation in adherence and ingestion of Staphylococcus aureus (645% of control) and of C3b receptor (CR1) expression (292% of control) and a slight increase in hexose monophosphate shunt activity without changing cell growth rates or Fc fragment receptor expression. The changes in cellular association of S. aureus and the CR1 were detected as early as 48 hr of incubation and peaked between 3 and 5 days. Similar changes in the CR1 were induced by 25-hydroxy- and 24,25-dihydroxyvitamin D3 at micromolar concentrations. Dexamethasone, hydrocortisone, and progesterone had no effect on CR1 expression. U937 cells incubated in the presence of vitamin D metabolites exhibited a change in their phenotype. These results suggest that vitamin D metabolites may contribute to monocyte/macrophage differentiation.

Calcifediol↗

PubMed1994

[The role of TNF-alpha in the growth and differentiation of U937 cells induced by PMA and IFN-gamma].

The effects of PMA and IFN-gamma on regulation of growth and differentiation of human monoblastic leukemic cell U937 were examined. U937 cells were stimulated by different concentrations of PMA and IFN-gamma respectively and NBT reduction assay was used to detect the differentiation of the cells. The results showed that both PMA and IFN-gamma dose-dependently induced differentiation of U937 cells into mature macrophage-like cells. The data also revealed a time-course response in the differentiation induction. Moreover, the U937 cell growth was significantly inhibited by the treatment of PMA and IFN-gamma. These results suggest that PMA and IFN-gamma coupled the regulation of U937 cell growth and differentiation. It was found that tumor necrosis factor-alpha (TNF-alpha) was expressed by the stimulated U937 cells. The specific monoclonal antibody against TNF-alpha diminished the effects of PMA and IFN-gamma on the growth and differentiation of U937 cells. Thus the endogenous TNF-alpha may involved in the mechanism of the effects of PMA and IFN-gamma on the differentiation of U937 cells. The regulatory action of the endogenous TNF-alpha on U937 cells was not due to its cytotoxic effect.

Cell Transformation, Neoplastic↗

PubMed1999

Phorbol ester inhibits DNA damage-induced apoptosis in U937 cells through activation of protein kinase C.

The effects of phorbol 12-myristate 13-acetate (PMA) on DNA damage-induced apoptosis were examined in promyelocytic leukemia cells, U937, in comparison with other differentiation-inducing agents to clarify the role of protein kinase C (PKC) vis-a-vis cellular differentiation in apoptosis. The apoptosis of U937 cells was observed at as early as 1-1.5 h following UV irradiation, with most cells being in apoptotic state at 3 h. Pretreatment with PMA for as short as 5 min was sufficient to inhibit apoptosis induced by UV irradiation, whereas apparent changes in cell cycle distributions and expression of differentiation markers by PMA were not observed until 12 h and 48 h, respectively. The inhibition of apoptosis by PMA was completely abolished by the pretreatment with calphostin C, a PKC inhibitor, and 4 alpha-phorbor 12,13-didecanoate, which is unable to activate PKC, did not protect U937 cells against apoptosis induced by UV irradiation. Other differentiation inducers, such as cyclic AMP and active vitamin D3, did not affect the UV-induced apoptosis of U937 cells. Taken together, it was suggested that PMA inhibits DNA damage-induced apoptosis through the activation of PKC rather than as a result of differentiation of U937 cells.

Apoptosis↗

PubMed2005

Quercetin arrests G2/M phase and induces caspase-dependent cell death in U937 cells.

Quercetin, a natural product derived from grapes, has been shown to prevent carcinogenesis in murine models. We report here that quercetin induces anti-proliferation and arrests G2/M phase in U937 cells. The G2/M phase accumulation was accompanied by an increase in the level of the cyclin B. In contrast, the level of the cyclin D, cyclin E, E2F1, and E2F2 was marked decreased in quercetin-treated U937 cells. Removal of quercetin from the culture medium stimulates U937 cells to synchronously re-enter the cell cycle, decrease expression level of cyclin B, and increased the expression level of cyclin D and cyclin E. These data demonstrate that quercetin causes reversible G2/M phase arrest, which was related with dramatic changes in the level of cyclin B, cyclin D, and cyclin E. Quercetin-induced down-regulation of cyclin D and cyclin E was associated with suppression of transcriptional levels but not protein stability. In addition, quercetin-treated U937 cells showed DNA fragmentation, increased sub-G1 population, and generated a 60kDa cleavage product of PLC-gamma1 in a dose-dependent manner, which were significantly inhibited by z-VAD-fmk. These data clearly indicate that quercetin-induced apoptosis is associated with caspase activation. In summary, the growth inhibition of the quercetin is highly related to cell cycle arrest at the G2/M phase and induction of caspase-dependent apoptosis in human promonocytic U937 cells.

Apoptosis↗

PubMed2003

Proteomic studies of macrophage-derived foam cell from human U937 cell line using two-dimensional gel electrophoresis and tandem mass spectrometry.

SUMMARY: The authors have identified 37 proteins in the whole-cell extracts from human monoblastic leukemia (U937) cell and macrophage-derived foam cell. The in vitro foam cell model was established by incubating the human U937 cells with oxidized low-density lipoprotein. The global changes in protein expressions between U937 foam cell and normal U937 cells were measured with two-dimensional polyacrylamide gel electrophoresis, and some proteins were trypsin-digested and then identified through tandem mass spectrometry after capillary liquid chromatography separation. Some of the identified proteins were validated via Internet links to the U937 proteomic map provided on the Expasy proteomics server. The experimental data can provide potential markers for atherosclerotic studies.

Electrophoresis, Gel, Two-Dimensional↗

PubMed1996

Augmentation of interferon production after cell-differentiation of U937 cells by TPA.

Persistent infections with mumps virus were established in several human lymphoid cells of T-cell origin (Molt-4, TALL-1, and CCRF-CEM) and human monocyte cells (U937 and THP-1). 2',5'-Oligoadenylate synthetase (2-5AS) activity was demonstrated to be only slightly induced by interferon (IFN) or TPA (12-O-tetradecanoyl-phorbol-13-acetate) treatment in these cells. Treatment of the persistently infected cells with IFN or TPA did not stimulate an increase in the amount of synthetase mRNA. Induction of cell differentiation and augmentation of IFN production by TPA were demonstrated in U937 cells persistently infected with mumps virus (U937-MP). Similar results for IFN production were obtained from differentiated U937 cells. It is suggested that cell differentiation of U937 cells might be associated with the development of IFN inducibility.

2',5'-Oligoadenylate Synthetase↗

PubMed2006

Antioxidant enzyme inhibitors enhance nitric oxide-induced cell death in U937 cells.

Nitric oxide (NO), a radical species produced by many types of cells, is known to play a critical role in many regulatory processes, yet it may also participate in collateral reactions at higher concentrations, leading to cellular oxidative damage. The protective role of antioxidant enzymes against NO-induced oxidative damage in U937 cells was investigated in control and cells pre-treated with diethyldithiocarbamic acid, aminotriazole, and oxlalomalate, specific inhibitors of superoxide dismutase, catalase, and NADP(+)-dependent isocitrate dehydrogenase, respectively. Upon exposure to 1 mM S-nitroso-N-acetylpenicillamine (SNAP), the nitric oxide donor, to U937 cells, the viability was lower and the protein oxidation, lipid peroxidation and oxidative DNA damage reflected by an increase in 8-hydroxy-2'-deoxyguanosine, were higher in inhibitor-treated cells as compared to control cells. We also observed the significant increase in the endogenous production of reactive oxygen species, as measured by the oxidation of 2'7'-dichlorodihydrofluorescin as well as the significant decrease in the intracellular GSH level in inhibitor-treated U937 cells upon exposure to NO. Upon exposure to 0.2 mM SNAP, which induced apoptotic cell death, a clear inverse relationship was observed between the control and inhibitor-treated U937 cells in their susceptibility to apoptosis. These results suggest that antioxidant enzymes play an important role in cellular defense against NO-induced cell death including necrosis and apoptosis.

Amitrole↗

PubMed2001

Chemopreventive agent resveratrol, a natural product derived from grapes, reversibly inhibits progression through S and G2 phases of the cell cycle in U937 cells.

Resveratrol, a natural product derived from grapes, has been shown to prevent carcinogenesis in murine models. We report here that resveratrol induces antiproliferation and arrests the S phase in human histiocytic lymphoma U937 cells. Resveratrol induces arrest in the S phase at low concentrations (30-60 microM), but high concentrations do not induce S phase accumulation in U937 cells. Removal of resveratrol from the culture medium stimulates U937 cells to reenter the cell cycle synchronously, as judged by the expression patterns of cyclin E, A and by fluorescent activated cell sorting analysis. These data demonstrate that resveratrol causes S phase arrest and reversible cell cycle arrest. Thus, resveratrol provides an important new cell cycle blocker as well as a cancer chemopreventive agent.

Antineoplastic Agents, Phytogenic↗

PubMed2007

Antioxidant enzyme inhibitors enhance peroxynitrite-induced cell death in U937 cells.

Peroxynitrite, a potent physiological inorganic toxin, is known to play a critical role in cellular oxidative damage. The protective role of antioxidant enzymes against peroxynitrite-induced oxidative damage in U937 cells was investigated in control and cells pre-treated with diethyldithiocarbamic acid, aminotriazole, and oxlalomalate, specific inhibitors of superoxide dismutase, catalase, and NADP(+)-dependent isocitrate dehydrogenase, respectively. Upon exposure to 1 mM 3-morpholinosydnomine N-ethylcarbamide (SIN-1), a generator of peroxynitrite through the reaction between nitric oxide and superoxide anion, to U937 cells, the viability was lower and the protein oxidation, lipid peroxidation and oxidative DNA damage reflected by an increase in 8-hydroxy-2'-deoxyguanosine, were higher in the inhibitor-treated cells as compared to the control cells. We also observed the significant increase in the endogenous production of reactive oxygen species, as measured by the oxidation of 2'7'-dichlorodihydrofluorescin as well as the significant decrease in the intracellular GSH level in the inhibitor-treated U937 cells upon exposure to SIN-1. These results suggest that antioxidant enzymes play an important role in cellular defense against peroxynitrite-induced cell death.

Amitrole↗