Tumor necrosis factor type α (cachectin) stimulates mouse osteoblast-like cells (MC3T3-E1) to produce macrophage-colony stimulating activity and prostaglandin E2

Sato, Kanji; Kasono, Keizo; Fujii, Yuko; Kawakami, Masanobu; Tsushima, Takahiro; Shizume, Kazuo

doi:10.1016/0006-291x(87)91324-6

Cited by 79 publications

(34 citation statements)

References 18 publications

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“…Osteopetrotic cells produced similar basal M-CSF levels as normal cells, however, because the response to IL-1␣ and TNF-␣ was different in our osteopetrotic primary osteoblastlike cells as compared to normal cells, or other osteoblast-like cells (22,23), the failure to respond normally to both cytokines may reflect the state of differentiation of these cells (as does the alkaline phosphatase activity and osteocalcin release observed in these cells), which failed to express either the necessary receptors for IL-1␣ or TNF-␣ pre-BMT, or expressed a postreceptor defect. A truncated, biologically inactive molecule of M-CSF may be responsible for this condition in the os- teopetrotic (op) mouse (24,40).…”

Section: Discussionmentioning

confidence: 73%

“…IL-1 ␣ and TNF-␣ are potent stimulators of bone resorption, and enhance the release of M-CSF by osteoblasts (22,23). Indeed, primary osteoblast-like cells produced M-CSF, and basal levels of M-CSF in osteopetrotic cell cultures were not significantly differ- Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Macrophage colony stimulation factor (M-CSF), which is necessary for the growth and differentiation of hematopoietic cells (20), is produced by osteoblast-like cells (21)(22)(23), cooperates with other factors such as interleukin-3 (IL-3) and -1 (IL-1) in the formation of osteoclasts, and may also be impaired in these animals (24).…”

Section: Introductionmentioning

confidence: 99%

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Demonstration of an osteoblast defect in two cases of human malignant osteopetrosis. Correction of the phenotype after bone marrow transplant.

Lajeunesse¹,

Busque²,

Ménard³

et al. 1996

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 73%

Section: Resultsmentioning

confidence: 99%

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Demonstration of an osteoblast defect in two cases of human malignant osteopetrosis. Correction of the phenotype after bone marrow transplant.

Lajeunesse¹,

Busque²,

Ménard³

et al. 1996

J. Clin. Invest.

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“…Furthermore, PGE2 treatment of murine peritoneal macrophages blocks LPS-induced expression of TNF mRNA (30). Previous studies in a murine osteoblast-like cell line have demonstrated that TNF stimulates production of PGE2 and macrophage-colony stimulating activity (39). However, while indomethacin abolished TNFinduced PGE2 production in these cells, there was little, if any, effect on induction of colony stimulating activity (39 …”

Section: Methodsmentioning

confidence: 93%

Transcriptional and posttranscriptional regulation of macrophage-specific colony stimulating factor gene expression by tumor necrosis factor. Involvement of arachidonic acid metabolites.

Sherman¹,

Weber²,

Datta³

et al. 1990

J. Clin. Invest.

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The effects of tumor necrosis factor (TNF) on the regulation of macrophage-specific colony stimulating factor (CSF-1) gene expression have been studied in HL-60 cells during monocytic differentiation. CSF-1 transcripts were undetectable in uninduced HL-60 cells, reached maximal levels by 3 h of exposure to TNF, and returned to that of control cells by 24 h. Transcriptional run-on analysis demonstrated that exposure to TNF stimulated the rate of CSF-I gene transcription by 6.4-fold. The combination of a protein synthesis inhibitor, cycloheximide, and TNF increased levels of CSF-I mRNA compared with treatment by TNF alone. We also studied the signal transduction mechanisms responsible for regulating TNF-induced CSF-I mRNA levels. Both 4-bromophenacyl bromide and quinacrine, inhibitors of phospholipase A2 activity, blocked TNF-induced increases in CSF-i transcripts in a concentration-dependent manner, while caffeic acid and nordihydroguaiaretic acid, inhibitors of the 5-lipoxygenase pathway, had no detectable effect on induction of CSF-1 RNA. PGE2 or dibutyryl cAMP treatment of HL-60 cells in the presence of TNF blocked the expression of CSF-1 mRNA in a dose-dependent manner. These findings suggest that the increase in CSF-I RNA observed during TNF treatment is regulated, at least in part, by both transcriptional and posttranscriptional mechanisms, and that PGE2 and cAMP regulate transcriptional activation of the CSF-1 gene by TNF. (J. Clin. Invest.

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“…Inhibition of prostaglandin production prevented the hypothermia and changes in blood glucose. Production of PgE2 is also enhanced after stimulation of mouse osteoblastlike cells (Sato et al, 1987) and endothelial cells (Dayer et al, 1985) with TNF-x. Both TNF-x and interleukin I have been shown to stimulate the production of PgE2 by isolated extensor digitorum longus muscles (Moldawer et al, 1987a Indomethacin administration decreases both the weight loss and dehydration after TNF-:x, suggesting that the anorectic effect is mediated through a prostaglandin intermediate.…”

Section: Discusiomentioning

confidence: 96%

Role of prostaglandins in tumour necrosis factor induced weight loss

Mahony

Tisdale²

1989

Br J Cancer

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SmmaryAdministration of either tumour necrosis factor alpha or 16,16-dimethylprostaglandin E2 (PGE2) to female NMRI mice caused a decrease in body weight accompanied by a reduction in both food and water intake and a decrease in carcass water content. A single injection of TNF-2 caused an enhanced production of PGE2 by spleen cells from treated animals, that was significant within I h of treatment, and persisted until at least 6h. These results suggest that the anorectic effect of TNF-z may be mediated by a prostaglandin intermediate. Indomethacin (lOmgkg-) administered 2h before TNF-a (7.5 x 107 U kg-') caused a significant reduction in the extent of weight loss and inhibited PgE2 production. Administration of indomethacin 0.5-1.5 h before the TNF-z had no significant effect on loss of body weight, but still inhibited PgE2 production. Also PgE2 production was still enhanced in response to TNF-2 administered chronically, despite the inability of prolonged TNF-z administration to produce continued loss of body weight. These results suggest that prostaglandins are not involved in the anorectic effect of TNF-z.The catabolic states associated with infection or endotoxemia have been attributed to the production by phagocytic cells of soluble proteins such as interleukin 1 and cachectin (Rouzer & Cerami, 1980;Moldawer et al., 1987a;Cerami et al., 1985). A high degree of homology has been shown to exist between the N-terminal sequence of mouse cachectin and the N-terminal sequence for human tumour necrosis factor-alpha (TNF-x) and the catabolic states have been extended to include also cancer-associated cachexia (Beutler & Cerami, 1986). Severe weight loss and increased mortality have been observed in mice bearing transgenic tumours that persistently secrete human cachectin (Oliff et al., 1987) and chronic administration of sublethal doses of TNF-x to rats caused anorexia, weight loss, depletion of body lipid and protein, a reduction of red blood cell mass, leukocytosis and tissue inflammation (Tracey et al., 1988). However, in a number of studies (Stovroff et al., 1988;) administration of TNF-x caused a loss in body weight accompanied by a drop in food and water intake, which was only apparent over the first 24h, after which animals became resistant to subsequent dosing. In addition TNF-x has not been detectable in the serum of patients with clinical cancer cachexia (Socher et al., 1988) and in clinical tnrals of recombinant human TNF-x there was no clinical evidence of accelerated cachexia, although anorexia was present during administration (Sherman et al., 1988). Also the effects on host metabolism produced by TNF-:x appear to differ from that produced by a cachexiainducing tumour .The toxic and metabolic effects of TNF-:z can be blocked by a single injection of the cyclo-oxygenase inhibitors indomethacin or ibuprofen before the TNF-x treatment (Kettlehut et al., 1987). This suggests that some of the effects of TNF-x may be mediated through a prostaglandin intermediate in analogy with septic shock where l...

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Tumor necrosis factor type α (cachectin) stimulates mouse osteoblast-like cells (MC3T3-E1) to produce macrophage-colony stimulating activity and prostaglandin E2

Cited by 79 publications

References 18 publications

Demonstration of an osteoblast defect in two cases of human malignant osteopetrosis. Correction of the phenotype after bone marrow transplant.

Demonstration of an osteoblast defect in two cases of human malignant osteopetrosis. Correction of the phenotype after bone marrow transplant.

Transcriptional and posttranscriptional regulation of macrophage-specific colony stimulating factor gene expression by tumor necrosis factor. Involvement of arachidonic acid metabolites.

Role of prostaglandins in tumour necrosis factor induced weight loss

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