The 55-kD tumor necrosis factor receptor on human keratinocytes is regulated by tumor necrosis factor-alpha and by ultraviolet B radiation.

Trefzer, Uwe; Brockhaus, Manfred; Lötscher, Hansruedi; Parlow, Frauke; Budnik, Anne; Grewe, Markus; Christoph, Hilmar; Kapp, Alexander; Schöpf, Erwin; Luger, Thomas A.

doi:10.1172/jci116589

Cited by 92 publications

(64 citation statements)

References 32 publications

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“…We demonstrated type I but not type II TNF-R gene expression in A549 cells by Northern blot analyses. Our results, as well as the findings of other researchers [30], support the concept that type I TNF-R is the dominant receptor in epithelial cells. These observations were not consistent with those of HIGUCHI and AGGARWAL [31], who noted type II TNF-R proteins in A549 cells; we do not know the precise reason for this discrepancy.…”

Section: Discussionsupporting

confidence: 92%

“…This evidence suggests that surface expression of TNF-R is regulated, at least in part, at the gene expression level. This type of modulation for TNF-R expression has been reported by others [30,[35][36][37], while our study seems to be the only report providing evidence that TNF downregulates the mRNA expression of its own receptor gene. It should be noted that this type of modulation needs several hours for protein synthesis.…”

Section: Discussionsupporting

confidence: 88%

See 1 more Smart Citation

Tumour necrosis factor receptor gene expression and shedding in human whole lung tissue and pulmonary epithelium

Nakamura¹,

Hino²,

Kato³

et al. 1996

Eur Respir J

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These results suggest that type I TNF-R gene expression and shedding of soluble TNF-R are differentially regulated in A549 cells. We conclude that tumour necrosis factor receptor surface expression is regulated, at least in part, at the gene expression level and shedding of soluble tumour necrosis factor receptor is modulated by inflammatory mediators, such as tumour necrosis factor in A549 cells.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 88%

Tumour necrosis factor receptor gene expression and shedding in human whole lung tissue and pulmonary epithelium

Nakamura¹,

Hino²,

Kato³

et al. 1996

Eur Respir J

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“…Hence, we cannot exclude that other putative receptors may be involved as well. However, TNF-R2, which also uses TRAF-2 for signaling, does not play a role since, like keratinocytes and other epithelial cells (33,42,43), HeLa cells do not express TNF-R2 (data not shown). In addition, activation of TNF-R1 appears to be a direct effect of UV and not due to autocrine release of TNF␣, since TNF␣ was not found increased in the supernatants of UV-exposed HeLa cells (data not shown).…”

Section: Discussionmentioning

confidence: 97%

Ultraviolet Radiation-induced Interleukin 6 Release in HeLa Cells Is Mediated via Membrane Events in a DNA Damage-independent Way

Kulms

Pöppelmann

Schwarz

2000

Journal of Biological Chemistry

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Evidence exists that ultraviolet radiation (UV) affects molecular targets in the nucleus or at the cell membrane. UV-induced apoptosis was found to be mediated via DNA damage and activation of death receptors, suggesting that nuclear and membrane effects are not mutually exclusive. To determine whether participation of nuclear and membrane components is also essential for other UV responses, we studied the induction of interleukin-6 (IL-6) by UV. Exposing HeLa cells to UV at 4°C, which inhibits activation of surface receptors, almost completely prevented IL-6 release. Enhanced repair of UV-mediated DNA damage by addition of the DNA repair enzyme photolyase did not affect UV-induced IL-6 production, suggesting that in this case membrane events predominante over nuclear effects. UV-induced IL-6 release is mediated via NFB since the NFB inhibitor MG132 or transfection of cells with a super-repressor form of the NFB inhibitor IB reduced IL-6 release. Transfection with a dominant negative mutant of the signaling protein TRAF-2 reduced IL-6 release upon exposure to UV, indicating that UV-induced IL-6 release is mediated by activation of the tumor necrosis factor receptor-1. These data demonstrate that UV can exert biological effects mainly by affecting cell surface receptors and that this is independent of its ability to induce nuclear DNA damage.

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“…interferon (IFN)-gamma, TNF-a p55 receptors), cytokines, growth factors, in¯ammatory mediators and adhesion molecules as well as activate transcription factors (e.g. NF-kB) (Dinarello et al, 1986;Scheurich et al, 1987;Doer¯er et al, 1989;Valyi-Nagy et al, 1992;Krakauer & Oppenheim, 1993;Trefzer et al, 1993;Mackay et al, 1993;Arias-Negrete et al, 1995;Schutze et al, 1995;Batten et al, 1996). This cytokine has been implicated in several in¯ammatory diseases (rheumatoid arthritis and Crohn's disease) and its inhibition has been the focus of many studies .…”

Section: Introductionmentioning

confidence: 99%

The effects of phosphodiesterase type 4 inhibitors on tumour necrosis factor‐α and leukotriene B₄ in a novel human whole blood assay

Brideau

Staden

Styhler

et al. 1999

British J Pharmacology

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1 The aim of this study was to assess the inhibitory activities of phosphodiesterase type 4 (PDE4) inhibitors on tumour necrosis factor-a (TNF-a) and leukotriene B 4 (LTB 4 ) production in a novel human whole blood assay. 2 Lipopolysaccharide (LPS) stimulation of human whole blood caused a time dependent increase in TNF-a and prostaglandin E 2 (PGE 2 ) plasma levels. Inhibition of LPS-induced TNF-a by the selective PDE4 inhibitor RP73401 was proportionally enhanced with endogenous PGE 2 (maximal after 24 h). In contrast, blocking endogenous PGE 2 production with indomethacin in blood stimulated with LPS for 24 h decreased the potency of RP73401 to that observed with a 4 h LPS incubation. 3 Non-selective and selective PDE4 inhibitors showed greater inhibition of LPS-induced TNF-a after 24 h compared to 4 h. Stereoselectivity was only achieved in the 24 h method. 4 LPS-stimulation of whole blood for either 30 min or 24 h followed by N-formyl-Met-Leu-Phe (fMLP) activation resulted in low plasma LTB 4 levels. Combination of both treatments resulted in a greater than 7 fold increase in plasma LTB 4 levels. Inhibition of the double LPS and fMLP-activated LTB 4 production was observed with non-selective and PDE4-selective inhibitors. Their LTB 4 inhibitory potencies were similar to that observed in the 24 h LPS-induced TNF-a assay. Thus, stimulation of human whole blood with two LPS stimulations followed by fMLP gives rise to both TNF-a and LTB 4 and their inhibition by various compounds can be assessed in the same blood sample. 5 Calcium ionophore (A23187) stimulation of whole blood resulted in plasma LTB 4 levels similar to the double LPS and fMLP method. Inhibition of A23187-induced LTB 4 biosynthesis was also achieved by PDE4-selective inhibitors as well as the direct 5-lipoxygenase (5-LO) inhibitor L-739,010. 6 These results con®rm the anti-in¯ammatory properties of PDE4 inhibitors. Thus, this novel human whole blood can be used to assess the biochemical e cacy of PDE4 inhibitors in human subjects.

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The 55-kD tumor necrosis factor receptor on human keratinocytes is regulated by tumor necrosis factor-alpha and by ultraviolet B radiation.

Abstract: IntroductionIn previous studies we showed that cultured human keratinocytes expressed the 55-kD TNF receptor (TNFR)

Cited by 92 publications

References 32 publications

Tumour necrosis factor receptor gene expression and shedding in human whole lung tissue and pulmonary epithelium

Tumour necrosis factor receptor gene expression and shedding in human whole lung tissue and pulmonary epithelium

Ultraviolet Radiation-induced Interleukin 6 Release in HeLa Cells Is Mediated via Membrane Events in a DNA Damage-independent Way

The effects of phosphodiesterase type 4 inhibitors on tumour necrosis factor‐α and leukotriene B₄ in a novel human whole blood assay

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The 55-kD tumor necrosis factor receptor on human keratinocytes is regulated by tumor necrosis factor-alpha and by ultraviolet B radiation.

Abstract: IntroductionIn previous studies we showed that cultured human keratinocytes expressed the 55-kD TNF receptor (TNFR)

Cited by 92 publications

References 32 publications

Tumour necrosis factor receptor gene expression and shedding in human whole lung tissue and pulmonary epithelium

Tumour necrosis factor receptor gene expression and shedding in human whole lung tissue and pulmonary epithelium

Ultraviolet Radiation-induced Interleukin 6 Release in HeLa Cells Is Mediated via Membrane Events in a DNA Damage-independent Way

The effects of phosphodiesterase type 4 inhibitors on tumour necrosis factor‐α and leukotriene B4 in a novel human whole blood assay

Contact Info

Product

Resources

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The effects of phosphodiesterase type 4 inhibitors on tumour necrosis factor‐α and leukotriene B₄ in a novel human whole blood assay