3,5,3'-triiodo-L-thyronine potentiates all-trans-retinoic acid-induced apoptosis during differentiation of the promyeloleukemic cell HL-60

Although the programmed cell death mediated by thyroid hormone is not well evaluated in mammalian cells, thyroid hormone plays a crucial role in differentiation of the cells during the metamorphosis of Xenopus, suggesting that thyroid hormone has the potential ability to induce the apoptosis. To inv...

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Bibliographic Details
Published in:Endocrinology (Philadelphia) 1997-02, Vol.138 (2), p.805-809
Main Authors: SUZUKI, S, KOBAYASHI, H, SEKINE, R, KUMAGAI, M, MIKOSHIBA, M, MORI, J.-I, HARA, M, ICHIKAWA, K, HASHIZUME, K
Format: Article
Language:English
Subjects:
Ageing, cell death
Apoptosis - drug effects
Biological and medical sciences
Cell Differentiation
Cell physiology
DNA Fragmentation
Drug Synergism
Fundamental and applied biological sciences. Psychology
HL-60 Cells - pathology
Humans
Kinetics
Molecular and cellular biology
Receptors, Thyroid Hormone - metabolism
Tretinoin - pharmacology
Triiodothyronine - pharmacology
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Summary:Although the programmed cell death mediated by thyroid hormone is not well evaluated in mammalian cells, thyroid hormone plays a crucial role in differentiation of the cells during the metamorphosis of Xenopus, suggesting that thyroid hormone has the potential ability to induce the apoptosis. To investigate the thyroid hormone-inducible apoptosis, we cultured HL-60 cells with various amounts of all-transretinoic acid (RA) and L-T3. T3 alone did not induce the apoptosis of the cells. T3, however, suppressed the proliferation of cells in the presence of RA. DNA ladder and microscopical examination showed that the reduction of cell number was due to the apoptosis induced by RA. These findings suggested that T3 affects the apoptotic process during the differentiation of HL-60 cells by RA. T3-inducible apoptosis may require the factors augmented by RA in HL-60 cells.
ISSN:0013-7227
1945-7170
DOI:10.1210/en.138.2.805