Functional macrophage cell lines transformed by abelson leukemia virus

Raschke, William C.; Baird, Stephen M.; Ralph, Peter; Nakoinz, Ilona

doi:10.1016/0092-8674(78)90101-0

Cited by 827 publications

(502 citation statements)

References 15 publications

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“…Unexpectedly, given the results with primary cells, we observed that E5531 was ineffective at inhibiting the early release of TNF-␣ from the RAW macrophage-like cell line. As an immortalized cell line, the RAW cells may have cellular responses that differ from those seen in primary macrophages (46). Immortalization may result in alterations in signal transduction pathways possibly involving NF-B and MAPKs, which could influence how these cells respond to external stimuli.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Toll-Like Receptor 4 by Lipopolysaccharide During Cellular Invasion by Live Salmonella typhimurium Is a Critical But Not Exclusive Event Leading to Macrophage Responses

Royle

Tötemeyer

Alldridge

et al. 2003

The Journal of Immunology

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Invasion of macrophages by salmonellae induces cellular responses, with the bacterial inducers likely to include a number of pathogen-associated molecular patterns. LPS is one of the prime candidates, but its precise role in the process, especially when presented as a component of live infecting bacteria, is unclear. We thus investigated this question using the lipid A antagonist E5531, the macrophage-like cell line RAW 264.7, and primary macrophage cultures from C3H/HeJ and Toll-like receptor 4−/− (TLR-4−/−) mice. We show that LPS presented on live salmonellae provides an essential signal, via functional TLR-4, for macrophages to produce NO and TNF-α. Furthermore, the mitogen-activated protein kinase c-Jun N-terminal kinase and p38 are activated, and the transcription factor NF-κB is translocated to the nucleus when RAW 264.7 cells are presented with purified LPS or live salmonellae. Purified LPS stimulates rapid, transitory mitogen-activated protein kinase activation that is inhibited by E5531, whereas bacterial invasion stimulates delayed, prolonged activation, unaffected by E5531. Both purified LPS and bacterial invasion caused translocation of NF-κB, but whereas E5531 always inhibited activation by purified LPS, activation by bacterial invasion was only inhibited at later time points. In conclusion, we show for the first time that production of NO and TNF-α is critically dependent on activation of TLR-4 by LPS during invasion of macrophages by salmonellae, but that different patterns of activation of intracellular signaling pathways are induced by purified LPS vs live salmonellae.

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Section: Discussionmentioning

confidence: 99%

Stimulation of Toll-Like Receptor 4 by Lipopolysaccharide During Cellular Invasion by Live Salmonella typhimurium Is a Critical But Not Exclusive Event Leading to Macrophage Responses

Royle

Tötemeyer

Alldridge

et al. 2003

The Journal of Immunology

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“…Activation of the c-Jun N-terminal kinase cascade and production of IL-1␤ in response to endotoxin have also been observed in this particular macrophage line (33) (R. D. Beigi, S. B. Kertesy, and G. R. Dubyak, unpublished observations). Most experiments and results described below were replicated using RAW 264.7 macrophages, another murine cell line widely used for studies of endotoxin signaling (6,7,(17)(18)(19)34).…”

Section: Endotoxin Signaling In Bac12f5 Macrophagesmentioning

confidence: 99%

Endotoxin Activation of Macrophages Does Not Induce ATP Release and Autocrine Stimulation of P2 Nucleotide Receptors

Beigi

Dubyak

2000

The Journal of Immunology

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Receptors for extracellular nucleotides (P2, or purinergic receptors) have previously been implicated in the transduction of endotoxin signaling in macrophages. The most compelling evidence has been the observation that inhibitors of ionotropic nucleotide (P2X) receptors, including periodate-oxidized ATP (oATP), attenuate a subset of endotoxin-induced effects such as activation of NF-κB and up-regulation of inducible NO synthase. We investigated whether endotoxin induces ATP release from a murine macrophage cell line (BAC1.2F5) using sensitive on-line assays for extracellular ATP. These cells constitutively released ATP, producing steady-state extracellular concentrations of ∼1 nM when assayed as monolayers of 106 adherent cells bathed in 1 ml of medium. However, the macrophages did not release additional ATP during either acute or prolonged endotoxin stimulation. In addition, cellular ecto-ATPase activities were measured following prolonged endotoxin activation and were found not to be significantly altered. Although oATP treatment significantly attenuated the endotoxin-induced production of NO, this inhibitory effect was not reproduced when the cells were coincubated with apyrase, a highly effective ATP scavenger. These results indicate that activation of macrophages by endotoxin does not induce autocrine stimulation of P2 nucleotide receptors by endogenous ATP released to extracellular compartments. Moreover, the data suggest that the ability of oATP to interfere with endotoxin signaling is due to its interaction with molecular species other than ATP-binding P2 receptors.

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“…We have reported the isolation of mutants, RAW.12 and RAW.108, derived from the macrophage-like cell line, RAW 264.7 [9], that are defective in the biosynthesis of ether lipids [10]. These mutants contain intact, functional peroxisomes.…”

Section: Introductionmentioning

confidence: 99%

Plasmalogens as endogenous antioxidants: somatic cell mutants reveal the importance of the vinyl ether

Zoeller

Lake

Nagan

et al. 1999

Biochemical Journal

179

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Exposure of plasmalogen-deficient variants of the murine cell line RAW 264.7 to short-term (0-100 min) treatment with electron transport inhibitors antimycin A or cyanide (chemical hypoxia) resulted in a more rapid loss of viability than in the parent strain. Results suggested that plasmalogen-deficient cells were more sensitive to reactive oxygen species (ROS) generated during chemical hypoxia ; the mutants could be rescued from chemical hypoxia by using the antioxidant Trolox, an α-tocopherol analogue, and they were more sensitive to ROS generation by plumbagin or by rose bengal treatment coupled with irradiation. In addition, the use of buffers containing #H # O greatly enhanced the cytotoxic effect of chemical hypoxia, suggesting the involvement of singlet oxygen. We used the unique enzymic deficiencies displayed by the mutants to differentially restore either plasmenylethanolamine (the major plasma-

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Functional macrophage cell lines transformed by abelson leukemia virus

Cited by 827 publications

References 15 publications

Stimulation of Toll-Like Receptor 4 by Lipopolysaccharide During Cellular Invasion by Live Salmonella typhimurium Is a Critical But Not Exclusive Event Leading to Macrophage Responses

Stimulation of Toll-Like Receptor 4 by Lipopolysaccharide During Cellular Invasion by Live Salmonella typhimurium Is a Critical But Not Exclusive Event Leading to Macrophage Responses

Endotoxin Activation of Macrophages Does Not Induce ATP Release and Autocrine Stimulation of P2 Nucleotide Receptors

Plasmalogens as endogenous antioxidants: somatic cell mutants reveal the importance of the vinyl ether

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