Lipopolysaccharide-stimulated TNF-α release from cultured rat Kupffer cells: sequence of intracellular signaling pathways

Lichtman, Steven N.; Wang, Jian; Lemasters, John J.

doi:10.1002/jlb.64.3.368

Cited by 26 publications

(20 citation statements)

References 16 publications

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“…5,6) The doses and effects of the inhibitors on the target signaling cascades were well examined in previous studies. 6,7) TiO 2 -concentration dependency of TNF-α release (particle size: 40 nm) was already examined in the Western blot analysis using anti-TNF-α antibody in Fig. 2, Inset in the present study, and also in other references.…”

Section: Methodssupporting

confidence: 56%

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Nanoscale Titanium Dioxide Particles Modulate Signaling Cascades for Tumor Necrosis Factor-.ALPHA. Release from Macrophages

Kim

Tao

2011

JOURNAL OF HEALTH SCIENCE

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Toxicological and biomedical effects of nanoparticles to living subjects should be elucidated before use for safety. To address this point, we attended to proinflammatory cytokine release from macrophagelike RAW 264.7 cells as a measure of the impact of nanoscale particles to living subjects. We explored the specific impacts of TiO 2 particles on the signaling cascades for proinflammatory cytokine and tumor necrosis factor-α (TNF-α release using a bioluminescent coculture system and an ELISA assay in the presence of various chemotherapeutic agents or biochemical inhibitors. This evaluation revealed that the proinflammatory cytokine release from the RAW 264.7 cells is synergically enhanced by the mixture of TiO 2 particles and interferon-γ (IFN-γ), and TNF-α release is modulated by 40 nm TiO 2 particles via a mitgen activated protein kinase (MAPK)/nuclear factor-kappa B (NF-κB) pathway. The TNF-α release is also affected by the agonist of glucocorticoid receptor in both basal and TiO 2 -particle-activated conditions. The present study evidences that nanoscale TiO 2 particles exert a modulator to the initial steps of inflammation, called TNF-α release from RAW 264.7 cells.

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Section: Methodssupporting

confidence: 56%

“…The inhibitor concentrations were referred from earlier papers. 6,7,10) The administered dose and expected inhibitory effects of the biochemical reagents inside cells are listed in Table 1. Ten minutes after pretreatment with the reagents, 40-nm TiO 2 particles were added to the wells to be 50 µg/ml.…”

Section: Methodsmentioning

confidence: 99%

Nanoscale Titanium Dioxide Particles Modulate Signaling Cascades for Tumor Necrosis Factor-.ALPHA. Release from Macrophages

Kim

Tao

2011

JOURNAL OF HEALTH SCIENCE

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“…12,13 Although cytochalasins have been used to block LPS uptake in several cell types, this molecule has also been shown to prevent downstream signaling as a consequence of LPS exposure. [32][33][34] Interestingly, Poussin et al 12 showed that cytochalasin D did not prevent LPS-dependent p38 MAPK and NF-B activation in THP-1 cells. In their study, cytochalasin D actually increased interleukin-8 secretion after LPS treatment.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide Internalization Activates Endotoxin-Dependent Signal Transduction in Cardiomyocytes

Cowan

Noria

Stamm

et al. 2001

Circulation Research

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Abstract-We tested the hypothesis that bacterial lipopolysaccharide (LPS) must be internalized to facilitate endotoxindependent signal activation in cardiac myocytes. Fluorescently labeled LPS was used to treat primary cardiomyocyte cultures, perfused heart preparations, and the RAW264.7 macrophage cell line. Using confocal microscopy and spectrofluorometry, we found that LPS was rapidly internalized in cardiomyocyte cultures and Langendorff-perfused hearts. Although LPS uptake was also observed in macrophages, only a fraction of these cells were found to internalize endotoxin to the extent seen in cardiomyocytes. Colocalization experiments with organelle or structure-specific fluorophores showed that LPS was concentrated in the Golgi apparatus, lysosomes, and sarcomeres. Similar intracellular localization was demonstrated in cardiomyocytes by transmission electron microscopy using gold-labeled LPS. The internalization of LPS was dependent on endosomal trafficking, because an inhibitor of microfilament reorganization prevented uptake in both cardiomyocytes and whole hearts. Inhibition of endocytosis specifically restricted early activation of extracellular signal-regulated kinase proteins and nuclear factor-B as well as later tumor necrosis factor-␣ production and inducible nitric oxide synthase expression.In conclusion, we have demonstrated that bacterial endotoxin is internalized and transported to specific intracellular sites in heart cells and that these events are obligatory for activation of LPS-dependent signal transduction. (Circ Res. 2001;88:491-498.)

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“…A time lapse of 15 to 30 min between LPS binding and LPS-induced responses such as cytokine release and adhesion was observed, which suggests that a time-consuming process such as internalization is necessary to enable signaling (93,315). Indeed, several, but not all, studies have revealed that blocking internalization or endosome fusion also blocks LPS-induced signaling (93,315,427,431). Although the precise mechanisms are not completely understood, it has been shown that monomeric LPS is transported into the cell to the Golgi complex, thus activating the cell.…”

Section: Cd14mentioning

confidence: 99%

Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock

2003

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Bacterial sepsis and septic shock result from the overproduction of inflammatory mediators as a consequence of the interaction of the immune system with bacteria and bacterial wall constituents in the body. Bacterial cell wall constituents such as lipopolysaccharide, peptidoglycans, and lipoteichoic acid are particularly responsible for the deleterious effects of bacteria. These constituents interact in the body with a large number of proteins and receptors, and this interaction determines the eventual inflammatory effect of the compounds. Within the circulation bacterial constituents interact with proteins such as plasma lipoproteins and lipopolysaccharide binding protein. The interaction of the bacterial constituents with receptors on the surface of mononuclear cells is mainly responsible for the induction of proinflammatory mediators by the bacterial constituents. The role of individual receptors such as the toll-like receptors and CD14 in the induction of proinflammatory cytokines and adhesion molecules is discussed in detail. In addition, the roles of a number of other receptors that bind bacterial compounds such as scavenger receptors and their modulating role in inflammation are described. Finally, the therapies for the treatment of bacterial sepsis and septic shock are discussed in relation to the action of the aforementioned receptors and proteins

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Lipopolysaccharide-stimulated TNF-α release from cultured rat Kupffer cells: sequence of intracellular signaling pathways

Cited by 26 publications

References 16 publications

Nanoscale Titanium Dioxide Particles Modulate Signaling Cascades for Tumor Necrosis Factor-.ALPHA. Release from Macrophages

Nanoscale Titanium Dioxide Particles Modulate Signaling Cascades for Tumor Necrosis Factor-.ALPHA. Release from Macrophages

Lipopolysaccharide Internalization Activates Endotoxin-Dependent Signal Transduction in Cardiomyocytes

Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock

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