Dexamethasone inhibits feedback regulation of the mitogenic activity of tumor necrosis factor, interleukin‐1, and epidermal growth factor in human fibroblasts

Kohase, Masayoshi; Henriksen‐DeStefano, Dorothy; Sehgal, Pravinkumar B.; Vilček, Ján

doi:10.1002/jcp.1041320211

Cited by 82 publications

(40 citation statements)

References 45 publications

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“…growth stimulation of FS4 cells by T N F has been described (37, 3x1. Under our assay conditions for [38,411, which are known to inhibit A4Ach release at least in some cells. Hence, the role of A4Ach in the growth stimulatory activity of T N F is still uncertain and controversial.…”

Section: Discussionmentioning

confidence: 98%

Tumour‐necrosis‐factor‐mediated cytotoxicity is correlated with phospholipase‐A₂ activity, but not with arachidonic acid release per se

Suffys

Beyaert

Valck

et al. 1991

European Journal of Biochemistry

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L929, a murine fibrosarcoma cell line highly sensitive to the anti-proliferative and cytotoxic action of tumour necrosis factor (TNF), was used as a target cell in our studies. We [Suffys et al. (1987) Biochem. Biophys. Res. Commun. 149, 735 -7431, as well as others, have previously provided evidence that a phospholipase (PL), most probably a PL-A,-type enzyme, is likely to be involved in TNF-mediated cell killing. We now further document this conclusion and provide suggestive evidence that the enzyme activity specifically involved in TNF cytotoxicity differs from activities associated with the eventual cell death process itself or with non-toxic serum treatment. We also show that the 5,8,11,14-icosatetraenoic acid (arachidonic acid, A4Ach) released by PL, and possibly metabolized, is unlikely to be a key mediator of the TNF-mediated cytotoxicity. These conclusions are based on the following experimental findings.1. TNF treatment of cells, prelabelled for 24 h with [jH]A4Ach or [14C]A3Ach (A3Ach = 5,8,11-icosatrienoic acid) resulted in an early, time-dependent and concentration-dependent release of radioactivity in the supernatant preceding actual cell death. The extent of this response was moderate, albeit reproducible and significant. Analysis of the total lipid fraction from cells plus supernatant revealed that only release of arachidonic acid from phospholipids, but not its metabolization was induced by TNF. However, the release of less unsaturated fatty acids, such as linoleic acid (Lin) or palmitic acid (Pam), was not affected during the first hours after TNF addition.2. An L929 subclone, selected for resistance to TNF toxicity, was found to be defective in TNF-induced A4Ach liberation.3. Interleukin-1 (IL1) was not cytotoxic for L929 and did not induce release of A4Ach. 4. Release of A4Ach was not restricted to TNF; the addition of serum to the cells also induced release of fatty acids into the medium. In this case, however, there was no specificity, as all fatty acids tested, including Lin and Pam, were released.5. Inhibition of PL-A, activity by appropriate drugs markedly diminished TNF-induced A4Ach release and resulted also in a strong decrease in TNF-induced cytotoxicity.6. Other drugs, including serine protease inhibitors, which strongly inhibit TNF-induced cytotoxicity, also decreased the TNF-induced A,Ach release, whereas LiCl potentiated both TNF-mediated effects.7. Protection of cells against TNF toxicity by means of various inhibitors was not counteracted by addition of exogenous fatty acids, including A,Ach.8. We could not detect an increase in the amount of free inositol or any inositol phosphate after TNF treatment of cells, prelabelled with my~- [~H]inositol. This indicates that the phosphatidylinositol-specific PL-C is not involved in the TNF-induced fatty acid release. 9. Neither were we able to observe a decrease in fatty acid incorporation into phospholipids during TNF treatment. This excludes a decrease in acyltransferase activity as the reason for increased levels of free fatty acid...

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Section: Discussionmentioning

confidence: 98%

Tumour‐necrosis‐factor‐mediated cytotoxicity is correlated with phospholipase‐A₂ activity, but not with arachidonic acid release per se

Suffys

Beyaert

Valck

et al. 1991

European Journal of Biochemistry

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“…Glucocorticoids, a class of multifunctional anti-inflammatory drugs, are well known for their ability to potently inhibit the synthesis of various proinflammatory cytokines (19). Administration of dexamethasone inhibited TNF and IL-1 synthesis and improved survival in a murine model of septic shock (5).…”

Section: Pharmacological Modulation With Cytokine Synthesis Inhibitorsmentioning

confidence: 99%

“…We used two independent cytokine synthesis inhibitors, prednisolone (PSL) and an N-benzoyl-L-phenylalanine derivative, JTE-607, in the current study. Although PSL is an established anti-inflammatory glucocorticoid that inhibits both pro-and anti-inflammatory cytokine synthesis in monocytes (19), glucocorticoids also inhibit T lymphocyte production of cytokines, such as interleukin (IL)-2 and interferon (IFN)-␥ (32), phagocytosis, and the secretion of reactive oxygen species (ROS) by macrophages (6), which are pivotal to selfdefense. Accordingly, treatment with glucocorticoids may increase the risk of infection (1).…”

mentioning

confidence: 99%

Prior burn insult induces lethal acute lung injury in endotoxemic mice: effects of cytokine inhibition

Sasaki¹,

Fujishima²,

Iwamura

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…In the first assay, which measures the increase in total cell protein, 15 SMCs were plated on day 0 in a 96-well microtiter plate (Nunclon) in medium containing 10% FCS at 2,500 cells/well and were allowed to attach overnight. On the following day, control wells were processed immediately to determine the protein level at attachment as a baseline.…”

Section: Cell Proliferation Assaysmentioning

confidence: 99%

Inhibition of smooth muscle cell proliferation and experimental angioplasty restenosis by beta-cyclodextrin tetradecasulfate.

Herrmann

Okada

Hozakowska

et al. 1993

Arterioscler Thromb

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Heparin inhibits smooth muscle cell proliferation in vitro, a property that makes it potentially useful in preventing restenosis after angioplasty. Its utility in this setting is limited by the inability to use high doses (secondary to anticoagulant effects) and the need for subcutaneous administration. We tested the ability of 0-cyclodextrin tetradecasulfate (CDT), a nonanticoagulant synthetic heparin mimic, to inhibit smooth muscle cell proliferation in vitro and tested its efficacy when orally administered for the prevention of angioplasty restenosis in a rabbit atherosclerosis model. Vascular smooth muscle cells were cultured from rabbit aortas by the explant technique. Passaged cells were plated at low density in microtiter plates in the presence or absence of varying concentrations of heparin or CDT in culture medium containing 10% fetal calf serum. Using both 3 H-thymidine incorporation and total protein assays, both heparin and CDT caused a similar dose-dependent inhibition of proliferation. We next tested the effect of orally administered CDT in the prevention of restenosis in focal femoral artery arteriosclerotic lesions created in hypercholesterolemic New Zealand White rabbits by air-dessication endothelial injury and subsequent peripheral angioplasty. Animals were followed up for 1 month and were fed normal chow supplemented by tap water with or without CDT. In animals receiving the highest concentration of CDT (2 mg/mL drinking water), the percentage of arterial cross-sectional area with intimal hyperplasia decreased from 50.5±1.7% (control) to 26.9±2.2% (p<0.001), with the intimal/ medial ratio being decreased from 1.4±0.4 to 0.5±0.2 (p=0.056). Angiographically, the mean minimum lumen diameter measured 1 month after angioplasty was reduced more in control than in CDT animals (-22% versus -2%, p<0.05). The restenosis rate (denned as loss of &50% of the initial gain) was 75% in control animals and 25% in animals receiving CDT (p<0.05). We conclude that the heparin mimic CDT inhibits smooth muscle cell proliferation in vitro and that its oral administration reduces both intimal hyperplasia and angiographic evidence of restenosis in this rabbit model of angioplasty. {Arteriosclerosis and Thrombosis 1993;13:924-931) KEY WORDS • angioplasty • restenosis • smooth muscle cells • heparin R estenosis after percutaneous transluminal angioplasty remains the most important limitation of this procedure despite efforts to solve the problem both biologically and mechanically.

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Dexamethasone inhibits feedback regulation of the mitogenic activity of tumor necrosis factor, interleukin‐1, and epidermal growth factor in human fibroblasts

Cited by 82 publications

References 45 publications

Tumour‐necrosis‐factor‐mediated cytotoxicity is correlated with phospholipase‐A₂ activity, but not with arachidonic acid release per se

Tumour‐necrosis‐factor‐mediated cytotoxicity is correlated with phospholipase‐A₂ activity, but not with arachidonic acid release per se

Prior burn insult induces lethal acute lung injury in endotoxemic mice: effects of cytokine inhibition

Inhibition of smooth muscle cell proliferation and experimental angioplasty restenosis by beta-cyclodextrin tetradecasulfate.

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Dexamethasone inhibits feedback regulation of the mitogenic activity of tumor necrosis factor, interleukin‐1, and epidermal growth factor in human fibroblasts

Cited by 82 publications

References 45 publications

Tumour‐necrosis‐factor‐mediated cytotoxicity is correlated with phospholipase‐A2 activity, but not with arachidonic acid release per se

Tumour‐necrosis‐factor‐mediated cytotoxicity is correlated with phospholipase‐A2 activity, but not with arachidonic acid release per se

Prior burn insult induces lethal acute lung injury in endotoxemic mice: effects of cytokine inhibition

Inhibition of smooth muscle cell proliferation and experimental angioplasty restenosis by beta-cyclodextrin tetradecasulfate.

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Tumour‐necrosis‐factor‐mediated cytotoxicity is correlated with phospholipase‐A₂ activity, but not with arachidonic acid release per se

Tumour‐necrosis‐factor‐mediated cytotoxicity is correlated with phospholipase‐A₂ activity, but not with arachidonic acid release per se