2000
Role of Arachidonic Acid Metabolites in Effects of TNF-alfa on Proliferation, Viability, Differentiation and Apoptosis of Human Leukaemic Cell Line HL-60
ŠTIKA, Jiří; Jan VONDRÁČEK; Jiřina HOFMANOVÁ; Alois KOZUBÍK; Vladimír ŠIMEK et al.Základní údaje
Originální název
Role of Arachidonic Acid Metabolites in Effects of TNF-alfa on Proliferation, Viability, Differentiation and Apoptosis of Human Leukaemic Cell Line HL-60
Autoři
Vydání
First edition. České Budějovice, Cells II, s. 135-135, 2000
Nakladatel
Kopp nakladatelství
Další údaje
Jazyk
angličtina
Typ výsledku
Stať ve sborníku
Obor
30102 Immunology
Utajení
není předmětem státního či obchodního tajemství
Označené pro přenos do RIV
Ano
Kód RIV
RIV/00216224:14310/00:00003964
Organizační jednotka
Přírodovědecká fakulta
ISBN
80-7232-120-X
Změněno: 8. 1. 2002 15:22, Mgr. Jiří Štika, Ph.D.
Anotace
V originále
Tumor necrosis factor-a (TNF-a) has been found to reduce cellular proliferation and viability, and to induce apoptosis, as well as a partial differentiation. These effects could contribute to elimination of leukemic cells. Using human leukemic cell line HL-60 as a model, we administered cyclooxygenase (indomethacin) and lipoxygenase (MK-886) inhibitors together with TNF-a, in order to evaluate the possible role of prostaglandins and leukotrienes in these processes. The following methods were used to assess cell proliferation, differentiation and apoptosis: cells were counted with haemocytometer; apoptosis and cell cycle were quantified using flowcytometry and fluorescence microscopy; viability was detected by means of light microscopy and flowcytometry; differentiation was followed as nonspecific esterase activity. Our results indicate that indomethacin can potentiate TNF-a-induced apoptosis, resulting in the decrease of number of cells and their viability during simultaneous treatment with TNF-a. However, no effect of indomethacin on the TNF-a-induced differentiation was observed. MK-886 reduced proliferation and viability of HL-60 cells and induced their apoptosis. Similar effects were observed when it was administered in combination with TNF-a. MK-886 strongly potentiated differentiation after TNF-a treatment, but did not induce differentiation when administered alone. In conclusion, inhibition of leukotriene production could potentiate differentiation by TNF-a, while prostaglandins could play a negative role in proapoptotic effects of TNF-a.
Návaznosti
| GA524/99/0694, projekt VaV |
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