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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↗

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↗

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↗

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↗

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↗

PubMed1989

Association of alpha interferon production with natural killer cell lysis of U937 cells infected with human immunodeficiency virus.

Mononuclear leukocytes from human immunodeficiency virus (HIV)-seronegative and -seropositive homosexual men lysed HIV-infected U937 cells to a significantly greater degree than uninfected U937 cells. Depletion of cell subsets with monoclonal antibodies and complement indicated that the effector cells were primarily of the CD16+ phenotype. Acid-stable alpha interferon (IFN-alpha) production induced by the HIV-infected cells correlated with, although was not an absolute requisite for, preferential lysis of the infected targets. The activity of these CD16+, natural killer (NK) cells decreased in relation to the duration of HIV infection and the presence of acquired immunodeficiency syndrome. Pretreatment of peripheral blood mononuclear cells from HIV-seronegative subjects, but not HIV-seropositive men, with IFN-alpha or recombinant interleukin-2 enhanced lysis of both uninfected and HIV-infected U937 cells. These results suggest that IFN-alpha-associated, NK-like mechanisms are active in the cytotoxic response against HIV-infected cells and that HIV infection results in an early and progressive depression of such responses. Prospective investigations may be useful in determining the role of this NK cell response in the natural history and pathogenesis of HIV infection and the efficacy of therapeutic modalities.

Acquired Immunodeficiency Syndrome↗

PubMed1993

Prostaglandin E2 receptors of a human monocytic cell line, U937 cells.

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Cell Line↗

PubMed2001

Activation of natural interferon-alpha producing cells by apoptotic U937 cells combined with lupus IgG and its regulation by cytokines.

We recently demonstrated that IgG from patients with systemic lupus erythematosus (SLE) in combination with U937 cells made apoptotic by UV-irradiation, can induce interferon-alpha (IFN-alpha) production in normal peripheral blood mononuclear cells (PBMC). In the present study we show by flow cytometry that the actual IFN-alpha producing cells (IPC) among PBMC had the same phenotype (HLA-DR+, CD4+, CD11b-, CD11c-, CD14-, CD19-, CD32-, CD36+, CD40+, CD45RA+, CD68+, CD83+, CD86-, IL-3R+ and IL-10R-) and low frequency (approximately 2/10(4)PBMC) as the IPC activated by Herpes simplex virus type I. Consequently, these cells correspond to the natural IPC, also described as type 2 precursor dendritic cells. We also demonstrated that cytokines of possible importance in the pathogenesis in SLE had effects on the IFN-alpha production. Specifically, the IFN-alpha production was strongly increased by the type I IFNs, IFN-alpha and -beta, but markedly inhibited by IL-10 and also to some extent by TFN-alpha. In contrast, the cytokines IFN-gamma, IL-6, TGF-beta and GM-CSF had no clear effects. No production of IL-10 was detected in PBMC stimulated by apoptotic U937 cells and SLE IgG. These results may explain the cause of the ongoing IFN-alpha production in SLE patients and its relation to the autoimmune process.

Adolescent↗

PubMed1987

Effects of differentiation of human macrophage-like U937 cells on intrinsic resistance to herpes simplex virus type 1.

We have characterized the effect of differentiation on the resistance of the mononuclear phagocyte to herpes simplex virus type 1 (HSV-1) by using the human mononuclear phagocyte cell line, U937. The replication of HSV-1 was compared in undifferentiated U937 cells and U937 cells induced to undergo differentiation. Undifferentiated U937 cells were highly resistant to HSV-1 infection. Infectious virus levels declined rapidly to less than 0.1 plaque-forming units (PFU) per cell by 24 hr postinfection and the cells were completely resistant to HSV-1-induced cytopathic effect. Differentiation of U937 cells by treatment with phorbol 12-myristate 13-acetate (PMA) was accompanied by a decrease in the resistance to HSV-1 infection. Infectious virus yields were increased greater than 75-fold at 24 hr postinfection, as compared with the undifferentiated U937 cells. PMA-differentiated U937 cells also acquired full susceptibility to HSV-1-induced cytopathic effect. Infectious center assay revealed that the percent of productively infected cells increased from approximately 3% in undifferentiated U937 to greater than 50% in PMA-differentiated cells. U937 cells were also induced to differentiate by treatment with all-trans-retinoic acid, dimethyl sulfoxide, and lymphokine as shown by differentiation-associated changes in morphology and cytochemical enzymes. These cells, however, failed to display increased permissiveness for HSV-1, indicating that the change in permissiveness was uniquely associated with PMA treatment. Undifferentiated U937 cells adsorbed as much virus as PMA-differentiated cells, but immunofluorescence assays, as well as DNA hybridization analysis demonstrated that an early block in HSV-1 replication occurred in undifferentiated U937 cells, before synthesis of viral protein and DNA. PMA-induced differentiation of U937 cells appears to release an early block in HSV-1 replication that is present in undifferentiated U937 cells.

Cell Differentiation↗

PubMed1999

Involvement of N-acetylcysteine-sensitive pathways in ricin-induced apoptotic cell death in U937 cells.

We have found that the antioxidant N-acetylcysteine (NAC) strongly inhibited ricin-induced apoptotic cell death in U937 cells (human myeloid leukemia), as judged by cytotoxicity, nuclear morphological change, and DNA fragmentation. Consistent with these observations, a significant depletion of cellular glutathione was observed in ricin-treated cells, and NAC prevented the decrease in cellular glutathione. On the other hand, among the caspase inhibitors tested, Z-Asp-CH2-DCB, which inhibited ricin cytotoxicity, also suppressed ricin-mediated glutathione depletion, while NAC did not affect the generation of caspase-3 like activity in ricin-treated cells. These results suggest that glutathione loss takes place downstream from caspase activation during the ricin-induced apoptotic process. Treatment with a specific inhibitor of glutathione biosynthesis, buthionine sulfoximine (BSO) failed to induce apoptosis, and had no effect on the overall extent of ricin-induced apoptosis, even though the glutathione level was decreased to less than 5% of the control level. However, NAC still protected against ricin-induced apoptosis in the BSO-treated cells. We conclude that glutathione loss is one of several apoptotic changes caused by ricin, but is not a sufficient factor for the progress of apoptosis. NAC may prevent ricin-induced apoptosis through maintaining an intracellular reducing condition by acting as a thiol supplier.

Acetylcysteine↗

PubMed1994

Presence of a dysfunctional form of CD59 on a CD59+ subclone of the U937 cell line.

U937 cells are known to be relatively sensitive to C-mediated killing and have been reported to show variable expression of CD59. We have obtained stable CD59+ and CD59- sublines of the U937 cell line. Expression of other C-regulatory proteins, decay-accelerating factor (DAF), MCP and CR1, was similar on both cell lines. Although the sublines were morphologically similar and expressed similar amounts of most surface antigens, qualitative difference in expression of CD13 and CD64 and a quantitative difference in CD15 expression was observed. Sensitivity to C-mediated killing of the cell lines was measured using classical pathway activation. Both cell lines appeared to be equally sensitive to C-mediated killing. Monoclonal antibodies against CD59, which neutralize CD59 and enhance killing of most cell lines (including K562, HL60 and Molt4), did not enhance the killing of the CD59- cells but, surprisingly, also did not enhance killing of the CD59+ U937 subline. CD59 was expressed on the U937 subline at similar levels to that on HL60 and K562 cells, was glycosylphosphatidylinositol (GPI) anchored and could be immunoprecipitated from cell extracts. However, unlike these other cell lines, U937 cell extracts were negative in a Western blot using a variety of anti-CD59 antibodies even when ultrasensitive detection methods were used. These results indicate that the CD59+ U937 cell expresses a form of CD59 which is dysfunctional and structurally abnormal.

Animals↗