GM-CSF rescues TF-1 cells from growth factor withdrawal-induced, but not differentiation-induced apoptosis: The role of BCL-2 and MCL-1
GM-CSF rescues TF-1 cells from growth factor withdrawal-induced, but not differentiation-induced apoptosis: The role of BCL-2 and MCL-1
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DOI：
10.1006/cyto.1999.0514
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发表时间：
1999-11-01
期刊：
影响因子：
3.8
通讯作者：
Nimer, SD
中科院分区：
文献类型：
--
作者：
Klampfer, L;Zhang, J;Nimer, SD
粒细胞-巨噬细胞集落刺激因子(GM-CSF)和IL-3等细胞因子可促进造血细胞的存活和增殖。利用GM-CSF依赖的TF-1髓系白血病细胞株，发现停用GM-CSF后，内源性bcl2和mcl1水平下调，而bclx(L)和Bar水平不变。在TPA诱导的TF-1细胞分化过程中，BCL-2和MCL-1的表达不受调控，而在有GM-CSF存在的情况下，高表达BCL-2和MCL-1的TF-1细胞发生了延迟的凋亡，但对TPA没有影响。促红细胞生成素(EPO)诱导的TF-1细胞表达BCL-2和MCL-1蛋白。然而，这并不支持它们的长期增殖，进一步表明这些抗凋亡基因的上调不足以支持TF-1细胞的长期增殖。(C)1999年学术出版社。
Cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-3 promote the survival and stimulate the proliferation of haematopoietic cells. Using the GM-CSF-dependent TF-1 myeloid leukaemia cell line, the authors show that the endogenous levels of BCL-2 and MCL-1 are downregulated upon GM-CSF withdrawal, whereas the levels of BCL-x(L) and Bar are unchanged. Re-exposure of growth factor deprived cells to GM-CSF resulted in an early and transient increase in MCL-1 expression, and prolonged induction of BCL-2, which prevented apoptosis, In contrast, the expression of BCL-2 and MCL-1 were not modulated during TPA-induced differentiation of TF-1 cells, which was followed by apoptosis despite the presence of GM-CSF, TF-1 cells overexpressing BCL-2 or MCL-1 underwent delayed apoptosis upon growth factor withdrawal, but displayed no impaired apoptosis in response to TPA, Erythropoietin (Epo) induced the expression of BCL-2 and MCL-1 protein in TF-1 cells, however it did not support their long term proliferation, further demonstrating that upregulation of these anti-apoptotic genes is insufficient for the long term proliferation of TF-1 cells. (C) 1999 Academic Press.