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3,5,3'-Triiodo-L-Thyronine Potentiates All-Trans-Retinoic Acid-Induced Apoptosis during Differentiation of the Promyeloleukemic Cell HL-60

Department of Geriatrics, Endocrinology, and Metabolism, Shinshu University School of Medicine, Asahi, Matsumoto, Japan

Address all correspondence and requests for reprints to: Satoru Suzuki, M.D., Department of Geriatrics, Endocrinology, and Metabolism, Shinshu University School of Medicine, 3–1-1 Asahi, Matsumoto, Nagano 390, Japan. E-mail: rounen3{at}gipac.shinshu-u.ac.jp

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-trans-retinoic 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.

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