Apoptosis and DNA fragmentation precede TNF‐induced cytolysis in U937 cells

Wright, Susan C.; Kumar, Poornima; Tam, Albert W.; Shen, Naiping; Varma, Madhu; Larrick, James W.

doi:10.1002/jcb.240480403

Cited by 140 publications

(76 citation statements)

References 34 publications

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“…Samples were mounted and subjected to microscopic analysis. Nuclear condensation as revealed by DAPI staining in the absence of trypan blue uptake is considered characteristic of apoptosis as opposed to necrosis (14,15). The quantitative analysis included counting the number of apoptotic relative to all identifiable cells from at least 10 microscopic fields with an average of 70 cells per field.…”

Section: Apoptosis Assaysmentioning

confidence: 99%

Reverse Signaling Through Transmembrane TNF Confers Resistance to Lipopolysaccharide in Human Monocytes and Macrophages

Eißner

Kirchner

Lindner

et al. 2000

The Journal of Immunology

176

129

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We have previously reported that the CD14+ monocytic subpopulation of human PBMC induces programmed cell death (apoptosis) in cocultured endothelial cells (EC) when stimulated by bacterial endotoxin (LPS). Apoptosis is mediated by two routes, first via transmembrane TNF-α (mTNF) expressed on PBMC and, in addition, by TNF-independent soluble factors that trigger apoptosis in EC. Neutralizing anti-TNF mAb completely blocked coculture-mediated apoptosis, despite the fact that there should have been additional soluble cell death factors. This led to the hypothesis that a reverse signal is transmitted from the TNF receptor on EC to monocytes (MO) via mTNF that prevents the production of soluble apoptotic factors. Here we have tested this hypothesis. The results support the idea of a bidirectional cross-talk between MO and EC. Peripheral blood MO, MO-derived macrophages (MΦ), or the monocytic cell line Mono Mac 6 were preincubated with human microvascular EC that constitutively express TNF receptor type I (TNF-R1) and subsequently stimulated with LPS. Cell-free supernatants of these preparations no longer induced EC apoptosis. The preincubation of MO/MΦ with TNF-reactive agents, such as mAb and soluble receptors, also blocked the production of death factors, providing further evidence for reverse signaling via mTNF. Finally, we show that reverse signaling through mTNF mediated LPS resistance in MO/MΦ as indicated by the down-regulation of LPS-induced soluble TNF and IL-6 as well as IL-1 and IL-10.

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Section: Apoptosis Assaysmentioning

confidence: 99%

Reverse Signaling Through Transmembrane TNF Confers Resistance to Lipopolysaccharide in Human Monocytes and Macrophages

Eißner

Kirchner

Lindner

et al. 2000

The Journal of Immunology

176

129

View full text Add to dashboard Cite

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“…This finding is consistent with the findings for this cell line reported from our and other laboratories. 9,11 An apoptosis-inducing effect of the optimal concentration of TNF (10 ng/ml) was rapid and potent, and maximal effect was obtained at 2 days of incubation with TNF, when apoptosis by GM-CSF was significant (Figure 1b) but only minimal. Under these conditions, potent apoptosis-inducing effect of TNF was further potentiated by the simultaneous addition of GM-CSF with TNF ( Figure 2).…”

Section: Synergistic Induction Of Apoptosis By the Combination Of Gm-mentioning

confidence: 99%

Induction of apoptosis in human hematopoietic U937 cells by granulocyte–macrophage colony-stimulating factor: possible existence of caspase 3-like pathway

Okuma

Saeki

Shimura³

et al. 2000

Leukemia

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Granulocyte-macrophage colony-stimulating factor (GM-CSF) induced apoptosis in human hematopoietic U937 cells by itself and in a synergistic manner with tumor necrosis factor (TNF). GM-CSF-induced apoptosis was not inhibited by caspase inhibitors YVAD-CMK, DEVD-CHO and z-VAD-FMK, under the condition that these inhibitors potently suppressed TNFinduced apoptosis. Both GM-CSF and TNF induced caspase 3-like activity in this cell line though the time course was distinct between two cytokines, and combined stimulation of cells with GM-CSF plus TNF induced additive or synergistic activation of caspase 3-like activity. Amount of immunoreactive cleaved forms of caspase 3 recognized by specific antibody was completely dissociated with its enzymatic activity when the cells were stimulated with GM-CSF, but not with TNF. These results indicate that GM-CSF induces apoptosis of U937 cells via unknown pathway, which seems to be mediated by caspase 3-like activity, yet not caspase 3 itself, resistant to the caspase inhibitors, and synergistically interacts with conventional caspase 3 pathway of TNF. Possible involvement of caspases 1 and 8 (-like activity) but not caspase 7 in this pathway was also suggested. Leukemia (2000) 14, 612-619.

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“…The percentage of apoptotic cells was evaluated by a modification of the JAM test (Matzinger, 1991) and of the quantitative assay described by Wright et al (1992). Briefly, NB cells were treated or not with IFN-g, as described, in 24 well tissue culture plates.…”

Section: Quantitative Evaluation Of Apoptosismentioning

confidence: 99%

Induction of differentiation and apoptosis by interferon-γ in human neuroblastoma cells in vitro as a dual and alternative early biological response

et al. 1997

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Interferon-g (IFN-g) has a well known differentiation-promoting activity on several neuroblastoma (NB) cell lines and has also been reported to induce apoptosis in different cellular models. We have investigated the potential of IFN-g to trigger, besides differentiation, programmed cell death in NB cells and the relationship between these processes. Nine NB cell lines, characterized by different phenotypic and maturational features, were cultured in the presence of IFN-g (1000 IU/ml) for up to 5 days with either only one treatment at the start of the culture or renewing the culture medium (with or without IFN-g) every other day. Neuronal differentiation was assessed by evaluation of morphological changes and expression of mature cytoskeletal proteins, while apoptosis was evaluated at the desired times by fluorescent and electronic microscopy, DNA content analysis and DNA fragmentation assay. Our findings show that apoptosis is an early (mainly non postdifferentiative) event and is much more evident following a single IFN-g administration. Moreover, IFN-g-triggered apoptosis is independent of the cellular phenotype (schwannian or neuronal) and appears to be mutually exclusive with respect to differentiation at the single cell level. Our results strengthen the potential of IFN-g as a promising therapeutic agent for NB.

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Apoptosis and DNA fragmentation precede TNF‐induced cytolysis in U937 cells

Cited by 140 publications

References 34 publications

Reverse Signaling Through Transmembrane TNF Confers Resistance to Lipopolysaccharide in Human Monocytes and Macrophages

Reverse Signaling Through Transmembrane TNF Confers Resistance to Lipopolysaccharide in Human Monocytes and Macrophages

Induction of apoptosis in human hematopoietic U937 cells by granulocyte–macrophage colony-stimulating factor: possible existence of caspase 3-like pathway

Induction of differentiation and apoptosis by interferon-γ in human neuroblastoma cells in vitro as a dual and alternative early biological response

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