Role of NF?B in the regulation of macrophage colony stimulating factor by tumor necrosis factor-? in ST2 bone stromal cells

Isaacs, Scott; Fan, Xian; Fan, Dongjie; Gewant, H.; Murphy, Tamara C.; Farmer, Paul K.; Taylor, W. Robert; Nanes, Mark S.; Rubin, Janet

doi:10.1002/(sici)1097-4652(199905)179:2<193::aid-jcp9>3.0.co;2-3

Cited by 19 publications

(9 citation statements)

References 34 publications

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“…The human M‐CSF gene promoter was shown to be activated via its NF‐κB binding site in the presence of a pro‐inflammatory cytokine, TNF‐α, in HL60 cells (21) and in human osteoblast cells (22). On the other hand, using a mouse M‐CSF promoter construct, the TNF‐α‐induced NFκB p50/p60 complex formation did not stimulate the NF‐κB response element in the mouse stromal cell line St4 (23). Thus, the human M‐CSF gene promoter, but not mouse M‐CSF gene promoter, appears to be activated by inflammatory stimuli.…”

Section: Discussionmentioning

confidence: 95%

Macrophage‐Colony Stimulating Factor in Obese Adipose Tissue: Studies With Heterozygous op/+ Mice

Sugita¹,

Kamei²,

Oka³

et al. 2007

Obesity

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SUGITA, SATOSHI, YASUTOMI KAMEI, JUN-ICHIRO OKA, TAKAYOSHI SUGANAMI, AND YOSHIHIRO OGAWA. Macrophage-colony stimulating factor in obese adipose tissue: studies with heterozygous op/ϩ mice. Obesity. 2007;15:1988 -1995. Objective: We examined the gene expression of macrophage-colony stimulating factor (M-CSF) in mice with dietinduced obesity and in genetically obese mice. We also examined the effect of decreased M-CSF signaling on the susceptibility to obesity and macrophage recruitment into the adipose tissue of mice. Research Methods and Procedures:The adipose tissue from mice with diet-induced obesity, obese KKA y mice, and ob/ob obese mice was used for RNA preparation. Production of M-CSF and monocyte chemoattractant protein-1 (MCP-1) was examined by quantitative real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay. The op/ϩ heterozygous mice, with decreased functional M-CSF expression, were placed on a high-fat diet or crossed with KKA y mice to study the susceptibility to obesity. The gene expression of macrophage markers in adipose tissue was examined. Results: The expression of M-CSF was not significantly changed in mice on a high-fat diet or in either type of genetic obesity (KKA y or ob/ob mice). No change in the degree of obesity or macrophage-related gene expression (F4/80, CD68, and MCP-1) in the adipose tissue was observed in op/ϩ mice compared with ϩ/ϩ control mice, which were either treated with a high-fat diet or crossed with KKA y mice. Discussion: This study demonstrated that there was no significant change in the expression of M-CSF in the adipose tissue from obese mice and only a minor phenotypic change, such as macrophage infiltration, in the adipose tissue from op/ϩ mice, suggesting that M-CSF does not play a major role in macrophage recruitment in the adipose tissue of obese mice.

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Section: Discussionmentioning

confidence: 95%

Macrophage‐Colony Stimulating Factor in Obese Adipose Tissue: Studies With Heterozygous op/+ Mice

Sugita¹,

Kamei²,

Oka³

et al. 2007

Obesity

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“…4C, TRAP activity dose dependently increased in proportion to the added sOPGL. ST-2 cells express mMCSF in the absence of 1,25D or Dex, as we have previously shown (11). To assure that a lower level of mMCSF expression also supported osteoclastogenesis, sOPGL was added to cocultures of ST-2 cells and BMMs in the absence of 1,25D or Dex.…”

Section: Resultsmentioning

confidence: 99%

“…Many of these factors stimulate the expression of MCSF, leading to the hypothesis that the level of MCSF present within the local bone environment might dose dependently direct osteoclast formation. For instance, 1,25D, TNF-␣, and PTH, all of which potently induce osteoclast formation, cause increased secretion of sMCSF (11,24,31). Additionally, several investigators have suggested that estrogen deficiency might promote osteoclastogenesis by increasing the production of sMCSF by bone stromal cells (12,26).…”

Section: Discussionmentioning

confidence: 99%

“…However, very high levels of added sMCSF inhibit recruitment of progenitors into the osteoclast lineage despite increased proliferation of the predominant clone (6,20,29,34). Further confounding these issues is a lack of data demonstrating significant transcriptional control within the murine MCSF promoter by osteoclastogenic factors known to affect sMCSF expression (11,23). We and others have suggested that sMCSF secretion might be controlled posttranscriptionally (5) or posttranslationally via the trafficking of the secreted protein within the stromal cell (22).…”

Section: Discussionmentioning

confidence: 99%

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Increasing membrane-bound MCSF does not enhance OPGL-driven osteoclastogenesis from marrow cells

Fan

Gewant

et al. 2001

American Journal of Physiology-Endocrinology and Metabolism

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Macrophage colony-stimulating factor (MCSF) and osteoprotegerin ligand (OPGL), both produced by osteoblasts/stromal cells, are essential factors for osteoclastogenesis. Whether local MCSF levels regulate the amount of osteoclast formation is unclear. Two culture systems, ST-2 and Chinese hamster ovary-membrane-bound MCSF (CHO-mMCSF)-Tet-OFF cells, were used to study the role of mMCSF in osteoclast formation. Cells from bone marrow (BMM) or spleen were cultured with soluble OPGL on glutaraldehyde-fixed cell layers; osteoclasts formed after 7 days. Osteoclast number was proportional to the amount of soluble OPGL added. In contrast, varying mMCSF levels in the ST-2 or CHO-mMCSF-Tet-OFF cell layers, respectively by variable plating or by addition of doxycycline, did not affect BMM osteoclastogenesis: 20-450 U of mMCSF per well generated similar osteoclast numbers. In contrast, spleen cells were resistant to mMCSF: osteoclastogenesis required > or = 250 U per well and further increased as mMCSF rose higher. Our results demonstrate that osteoclast formation in the local bone environment is dominated by OPGL. Increasing mMCSF above basal levels does not further enhance osteoclast formation from BMMs, indicating that mMCSF does not play a dominant regulatory role in the bone marrow.

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“…It has been shown that pretreatment with the antioxidant agent N-acetylcysteine suppresses LPSmediated production of TNF-a and PGE2 by resident lung macrophages and that NAC suppresses NF-k B activation associated with reactive oxygen species (Mendez et al 1995, Fox et al 1997, Isaacs et al 1999, Li et al 2000. NF-k B activation is a critical convergence point of the in ammatory, cytotoxic and cytokine/TNF-a expression modulating pathways (Schreck et al 1992).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of polymethylmethacrylate particle-induced monocyte activation and IL-1β and TNF-α expression by the antioxidant agent N-acetylcysteine

Mulhall¹,

Given²

2002

Acta Orthopaedica Scandinavica

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We investigated the effectiveness of an antioxidant agent, N-acetylcysteine (NAC), in suppressing macrophage activation and mediator release in response to particulate debris. Polymethylmethacrylate (PMMA) particle-stimulated monocyte-macrophages were cultured alone and with varying concentrations of NAC. Tumor necrosis factor a (TNFa) and interleukin-1b (IL-1b) expression in the resultant cultures were measured using enzyme-linked immunosorbant assays. The ultrastructural effect of treatment was also assessed by electron microscopy. Cell viability in the various cultures was measured to rule out an effect of cytotoxicity. NAC treatment reduced TNFa and IL-1b expression by the monocyte-macrophages. Culturing with NAC was also associated with less ultrastructural activation of the monocytes. Furthermore, NAC was not associated with any adverse effect on cell viability in the concentrations used. Our ndings demonstrate the effectiveness of the antioxidant N-acetylcysteine in suppressing the cell activation and TNFa release seen on exposure to wear debris. This represents a novel potential therapeutic method in the prevention or treatment of periprosthetic osteolysis.

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Role of NF?B in the regulation of macrophage colony stimulating factor by tumor necrosis factor-? in ST2 bone stromal cells

Cited by 19 publications

References 34 publications

Macrophage‐Colony Stimulating Factor in Obese Adipose Tissue: Studies With Heterozygous op/+ Mice

Macrophage‐Colony Stimulating Factor in Obese Adipose Tissue: Studies With Heterozygous op/+ Mice

Increasing membrane-bound MCSF does not enhance OPGL-driven osteoclastogenesis from marrow cells

Inhibition of polymethylmethacrylate particle-induced monocyte activation and IL-1β and TNF-α expression by the antioxidant agent N-acetylcysteine

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