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| Description
| - Various liver diseases lead to an extensive inflammatory response and release of pro-inflammatory cytokines, such as TNF-alpha. We investigated possible interactions of TNF-alpha with ligands of the AhR receptor and known liver carcinogens, such as 2,3,7,8-TCDD and co-planar PCB 126. TNF-alpha significantly potentiated proliferative effects of picomolar range doses of both TCDD and PCB 126, leading to an increase in cell numbers, as well as an increased percentage of cells entering the S-phase of the cell cycle. The combination of TNF-alpha with low concentrations of AhR ligands increased both mRNA and protein levels of cyclin A. TNF-alpha temporarily inhibited AhR-dependent induction of CYP1A1. In contrast, TNF-alpha significantly enhanced induction of CYP1B1. These results suggest that TNF-alpha can significantly amplify effects of AhR ligands on deregulation of cell proliferation control, as well as on expression of CYP1B1, involved in metabolic activation of a number of mutagenic compounds.
- Various liver diseases lead to an extensive inflammatory response and release of pro-inflammatory cytokines, such as TNF-alpha. We investigated possible interactions of TNF-alpha with ligands of the AhR receptor and known liver carcinogens, such as 2,3,7,8-TCDD and co-planar PCB 126. TNF-alpha significantly potentiated proliferative effects of picomolar range doses of both TCDD and PCB 126, leading to an increase in cell numbers, as well as an increased percentage of cells entering the S-phase of the cell cycle. The combination of TNF-alpha with low concentrations of AhR ligands increased both mRNA and protein levels of cyclin A. TNF-alpha temporarily inhibited AhR-dependent induction of CYP1A1. In contrast, TNF-alpha significantly enhanced induction of CYP1B1. These results suggest that TNF-alpha can significantly amplify effects of AhR ligands on deregulation of cell proliferation control, as well as on expression of CYP1B1, involved in metabolic activation of a number of mutagenic compounds. (en)
- Různé jaterní choroby vedou k rozsáhlé zánětlivé odpovědi a uvolnění řady prozánětlivých cytokinů, jako je TNF-alfa. Zabývali jsme se možnými interakcemi TNF-alfa s ligandy receptoru AhR a známými jaterními karcinogeny, jako je 2,3,7,8-TCDD a koplanární PCB 126. TNF-alfa významně zesiloval proliferační účinky pikomolárních koncentrací TCDD i PCB 126, což vedlo k nárustu počtu buněk a zvýšenému procentu buněk vstupujících do S-fáze buněčného cyklu. Kombinace TNF-alfa s nízkými koncentracemi ligandů AhR zvyšovala hladinu cyklinu A na úrovni mRNA i proteinu. TNF-alfa dočasně inhiboval AhR-dependentní indukci cytochromu 1A1. Naproti tomu, TNF-alfa významně zvyšoval indukci CYP1B1. Tyto výsledky naznačují, že TNF-alfa může významně zesilovat účinky ligandů AhR na deregulaci kontroly buněčné proliferace, stejně jako účinky na expresi CYP1B1, který je zahrnut v metabolické aktivaci řady mutagenních sloučenin. (cs)
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| Title
| - Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome P450 enzymes in rat liver 'stem-like' cells
- TNF-alfa moduluje efekty ligandů receptoru AhR na buněčnou proliferaci a expresi enzymů cytochromů P450 v potkaních jaterních 'stem-like' buňkách (cs)
- Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome P450 enzymes in rat liver 'stem-like' cells (en)
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| skos:prefLabel
| - Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome P450 enzymes in rat liver 'stem-like' cells
- TNF-alfa moduluje efekty ligandů receptoru AhR na buněčnou proliferaci a expresi enzymů cytochromů P450 v potkaních jaterních 'stem-like' buňkách (cs)
- Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome P450 enzymes in rat liver 'stem-like' cells (en)
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| skos:notation
| - RIV/00027162:_____/07:#0000283!RIV08-MZE-00027162
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| http://linked.open.../vavai/riv/strany
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| http://linked.open...avai/riv/aktivita
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| http://linked.open...avai/riv/aktivity
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| http://linked.open...iv/cisloPeriodika
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| http://linked.open...vai/riv/dodaniDat
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| http://linked.open...aciTvurceVysledku
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| http://linked.open.../riv/druhVysledku
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| http://linked.open...iv/duvernostUdaju
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| http://linked.open...titaPredkladatele
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| http://linked.open...dnocenehoVysledku
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| http://linked.open...ai/riv/idVysledku
| - RIV/00027162:_____/07:#0000283
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| http://linked.open...riv/jazykVysledku
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| http://linked.open.../riv/klicovaSlova
| - cell proliferation; tumor necrosis factor-alpha; aryl hydrocarbon receptor; polychlorinated biphenyl; dioxin; xenobiotic metabolizing enzymes (en)
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| http://linked.open.../riv/klicoveSlovo
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| http://linked.open...odStatuVydavatele
| - GB - Spojené království Velké Británie a Severního Irska
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| http://linked.open...ontrolniKodProRIV
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| http://linked.open...i/riv/nazevZdroje
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| http://linked.open...in/vavai/riv/obor
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| http://linked.open...ichTvurcuVysledku
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| http://linked.open...cetTvurcuVysledku
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| http://linked.open...UplatneniVysledku
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| http://linked.open...v/svazekPeriodika
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| http://linked.open...iv/tvurceVysledku
| - Umannová, Lenka
- Vondráček, Jan
- Machala, Miroslav
- Krčmář, Pavel
- Kozubík, A.
- Zatloukalová, Jiřina
- Májková, Z.
- Hennig, B.
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| http://linked.open...n/vavai/riv/zamer
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