Yen A, Brown D, Fishbaugh J
Department of Internal Medicine, University of Iowa, Iowa City 52242.
Exp Cell Res. 1987 Nov;173(1):80-4. doi: 10.1016/0014-4827(87)90333-8.
The possible relationship of the pathways by which two inducers, retinoic acid and DMSO, cause myeloid differentiation of HL-60 promyelocytic leukemia cells was studied. HL-60 cells were first exposed to retinoic acid and then washed free of it. As reported previously, this brief exposure results in no subsequent G0 growth arrest or phenotypic differentiation. When these cells were subsequently exposed to DMSO, onset of G1/0 growth arrest but not phenotypic differentiation occurred within 24 h. Since in these cells retinoic acid or DMSO normally requires 48 h of continuous exposure for onset of significant G0 growth arrest and phenotypic differentiation, it appears that retinoic acid and DMSO induce similar early cellular events needed for subsequent G0 growth arrest but not for phenotypic differentiation. While onset of growth arrest and differentiation occur together when the cells are exposed for 48 h to retinoic acid, the present results indicate that their occurrence can be uncoupled by this split dosage to inducers. The results are discussed in terms of a previously hypothesized model of cellular response to the inducers.
研究了维甲酸和二甲基亚砜（DMSO）这两种诱导剂促使HL-60早幼粒细胞白血病细胞发生髓系分化的可能途径之间的关系。HL-60细胞首先暴露于维甲酸，然后洗去维甲酸。如先前报道，这种短暂暴露不会导致随后的G0期生长停滞或表型分化。当这些细胞随后暴露于DMSO时，在24小时内出现了G1/0期生长停滞，但未出现表型分化。由于在这些细胞中，维甲酸或DMSO通常需要连续暴露48小时才会出现显著的G0期生长停滞和表型分化，因此似乎维甲酸和DMSO诱导了随后G0期生长停滞所需的相似早期细胞事件，但不是表型分化所需的事件。当细胞暴露于维甲酸48小时时，生长停滞和分化同时发生，但目前的结果表明，通过这种对诱导剂的分次给药，它们的发生可以被分开。根据先前假设的细胞对诱导剂反应的模型对结果进行了讨论。
