Effects of tumor necrosis factor on cell growth and expression of transferrin receptors in human fibroblasts.

Hori, Takamitsu; Kashiyama, Satoshi; Oku, Naoto; Hayakawa, Makio; Shibamoto, Sayumi; Tsjimoto, Masafumi; Nishihara, Tatsuro; Ito, F.

doi:10.1247/csf.13.425

Cited by 14 publications

(4 citation statements)

References 31 publications

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“…T insulin, fibroblast growth factor, and 12-0-tetradecanoyl-phorbol-12-acetate did not (Hori et al, 1988). In this present study, TGF-P was also found to increase the growth of FS-4 cells.…”

Section: Discussionsupporting

confidence: 43%

Possible role of prostaglandins as negative regulators in growth stimulation by tumor necrosis factor and epidermal growth factor in human fibroblasts

Hori¹,

Kashiyama²,

Hayakawa³

et al. 1989

Journal Cellular Physiology

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Recombinant tumor necrosis factor (TNF), epidermal growth factor (EGF), and transforming growth factor beta (TGF-beta) stimulated growth of confluent human diploid fibroblasts (FS-4 cells) in the presence of fetal calf serum. TGF-beta synergistically enhanced both the TNF- and EGF-stimulated cell growth, whereas synergism between the mitogenic action of EGF and that of TNF was not observed. When indomethacin or acetylsalicylic acid, an inhibitor of prostaglandin production, was added to FS-4 cells, cell growth stimulated by EGF or TNF was increased, suggesting that prostaglandins induced by these mitogens antagonize their growth stimulatory actions. In contrast, neither indomethacin nor acetylsalicylic acid had a significant effect on the TGF-beta-induced growth of FS-4 cells. Mitogenic responses of indomethacin-treated cells to EGF, TNF, and TGF-beta were similarly suppressed by the addition of exogenous prostaglandin D2 (PGD2). Other prostaglandins such as PGE2 and PGF2 produced less inhibition of the cell growth.

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Section: Discussionsupporting

confidence: 43%

Possible role of prostaglandins as negative regulators in growth stimulation by tumor necrosis factor and epidermal growth factor in human fibroblasts

Hori¹,

Kashiyama²,

Hayakawa³

et al. 1989

Journal Cellular Physiology

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“…Reduction of TNF-induced PGE, synthesis by treatment with heparin was also observed when the experiment was carried out in the absence of fetal calf serum (Table 3, expt 2). The amounts of PGE, synthesized by cells in serum-free media were extremely low compared to that in media supplemented with fetal calf serum; previous observations have been made that fetal calf serum in the medium is an essential cofactor for TNF to exhibit certain types of biological functions (Hori et al, 1988;Sakagami et al, 1990;Martens et al, 1992).…”

Section: Surface-bound Type-11 Pla Is Involved In Pge Synthesismentioning

confidence: 93%

Participation in cellular prostaglandin synthesis of type‐II phospholipase A₂ secreted and anchored on cell‐surface heparan sulfate proteoglycan

Suga¹,

Murakami²,

Kudo³

et al. 1993

European Journal of Biochemistry

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Rat‐liver‐derived BRL‐3A cells, which express both type‐II phospholipase A2 (PLA2) and cytosolic PLA2 (cPLA2), generated prostaglandin E2 (PGE2) in the presence of fetal calf serum. When the cells were treated with tumor necrosis factor (TNF), PGE2 generation was greatly stimulated. The production of PGE2 observed in both cases was suppressed by a type‐II PLA2‐specific inhibitor, thielocin A1. Appreciable amounts of type‐II PLA2 were released into the medium from the TNF‐stimulated cells when heparin was added extracellularly. The release of type‐II PLA2 from TNF‐stimulated cells was also found in the presence of heparan sulfate or dextran sulfate, whereas other glycosaminoglycans showed no effects under the same conditions. These findings suggest that type‐II PLA2 expressed in BRL‐3A cells mostly associates with the cell surface by binding to cellular heparan sulfate proteoglycan. Removal of cell‐surface‐associated type‐II PLA2, by either extracellular addition of heparin or by prior treatment of the BRL‐3A cells with heparitinases, resulted in marked reduction of PGE2 synthesis in the cells. Exposure of BRL‐3A cells to thrombin also induced the apparent secretion of type‐II PLA2, and thrombin‐stimulated PGE2 generation was suppressed by heparin effectively. Type‐II PLA2 secreted and attached to heparan sulfate on the cell surface may therefore play an essential role in PGE2 synthesis by BRL‐3A cells.

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“…After several day's incubation, medium was removed and the cells were washed with CMF-PBS. Cell quantity was determined by the method of Hori et al (1988) with a minor modification. Cells were stained with 50 pl of 0.5% crystal violet per well in ethanoliwater (1:4) for 10 min and then washed with water.…”

Section: Automated Cell Countingmentioning

confidence: 99%

Apoptotic cell death induced by serum and its prevention by thiols

Kurita

Namiki

1994

Journal Cellular Physiology

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We recently reported that serum contains low molecular weight factors that inhibit growth and cause cell death in vitro. The present study focused on identifying components of basal media that counteract the toxic effects of serum. Amino acids L-cyst(e)ine and L-tryptophan were found to prevent serum-induced cell death of TIG-1 human fetal lung fibroblasts and other cell types. In addition to L-cysteine, other thiol-bearing and dithiol-cleaving compounds showed a similar ability to rescue the cells. Various inhibitors of protein or RNA synthesis also prevented the cell death. By contrast, nonthiol-containing reducing agents and super oxide dismutase (SOD), an active oxygen-eliminating enzyme, were ineffective. Thiol compounds appeared to exert a supportive level in TIG-1 cells cultured in FBS, whereas protein synthesis inhibitors did not alter the reduced intracellular thiol content. Fragmentation of DNA occurred prior to the plasma membrane breakdown of dying cells. Taken together, these data suggest that serum-induced cell death represents a form of apoptosis in which molecules containing thiol groups are active participants.

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Effects of tumor necrosis factor on cell growth and expression of transferrin receptors in human fibroblasts.

Cited by 14 publications

References 31 publications

Possible role of prostaglandins as negative regulators in growth stimulation by tumor necrosis factor and epidermal growth factor in human fibroblasts

Possible role of prostaglandins as negative regulators in growth stimulation by tumor necrosis factor and epidermal growth factor in human fibroblasts

Participation in cellular prostaglandin synthesis of type‐II phospholipase A₂ secreted and anchored on cell‐surface heparan sulfate proteoglycan

Apoptotic cell death induced by serum and its prevention by thiols

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Effects of tumor necrosis factor on cell growth and expression of transferrin receptors in human fibroblasts.

Cited by 14 publications

References 31 publications

Possible role of prostaglandins as negative regulators in growth stimulation by tumor necrosis factor and epidermal growth factor in human fibroblasts

Possible role of prostaglandins as negative regulators in growth stimulation by tumor necrosis factor and epidermal growth factor in human fibroblasts

Participation in cellular prostaglandin synthesis of type‐II phospholipase A2 secreted and anchored on cell‐surface heparan sulfate proteoglycan

Apoptotic cell death induced by serum and its prevention by thiols

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Product

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Participation in cellular prostaglandin synthesis of type‐II phospholipase A₂ secreted and anchored on cell‐surface heparan sulfate proteoglycan