Lipoxygenase metabolites are negative regulators of differentiation induced by tumor necrosis factor-alpha

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F01%3A00005223" target="_blank" >RIV/00216224:14310/01:00005223 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Lipoxygenase metabolites are negative regulators of differentiation induced by tumor necrosis factor-alpha

Popis výsledku v původním jazyce

Tumor necrosis factor-a (TNF) is a pleiotropic cytokine. Besides other effects it promotes differentiation of leukaemic cells and activates (phosphorylates) jun-NH2-terminal kinase (JNK). JNK activation might be involved in signalling pathway leading todifferentiation. MK-886 alone did not cause differentiation, however it increased non-specific esterase activity, reactive oxygen intermediates production and CD11b/CD14 cell surface antigen expression after TNF treatment, i. e. it potentiated differentiation of HL-60 cells. On the other hand indomethacin alone or in combination with TNF did not influence measured parameters of differentiation. Neither indomethacin, nor MK-886 influenced JNK activation. We concluded that endogenous LOX metabolites mightplay negative role in differentiation induced by TNF and that this effect is independent of JNK activation. These results may be beneficial for leukaemic patients.

Název v anglickém jazyce

Lipoxygenase metabolites are negative regulators of differentiation induced by tumor necrosis factor-alpha

Popis výsledku anglicky

Tumor necrosis factor-a (TNF) is a pleiotropic cytokine. Besides other effects it promotes differentiation of leukaemic cells and activates (phosphorylates) jun-NH2-terminal kinase (JNK). JNK activation might be involved in signalling pathway leading todifferentiation. MK-886 alone did not cause differentiation, however it increased non-specific esterase activity, reactive oxygen intermediates production and CD11b/CD14 cell surface antigen expression after TNF treatment, i. e. it potentiated differentiation of HL-60 cells. On the other hand indomethacin alone or in combination with TNF did not influence measured parameters of differentiation. Neither indomethacin, nor MK-886 influenced JNK activation. We concluded that endogenous LOX metabolites mightplay negative role in differentiation induced by TNF and that this effect is independent of JNK activation. These results may be beneficial for leukaemic patients.

Druh

D - Stať ve sborníku

CEP obor

ED - Fyziologie

OECD FORD obor

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Projekt

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Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2001

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název statě ve sborníku

2nd International Scientific Conference

ISBN

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ISSN

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e-ISSN

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Počet stran výsledku

1

Strana od-do

68

Název nakladatele

Univesity of Lviv, ukraine

Místo vydání

Lvov

Místo konání akce

Lvov

Datum konání akce

1. 1. 2001

Typ akce podle státní příslušnosti

WRD - Celosvětová akce

Kód UT WoS článku

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