Stat3-dependent induction of interleukin-3 receptor expression in leukemia inhibitory factor-stimulated M1 mouse leukemia cells
Stat3-dependent induction of interleukin-3 receptor expression in leukemia inhibitory factor-stimulated M1 mouse leukemia cells
复制标题
DOI：
10.1016/j.cyto.2003.10.009
复制
发表时间：
2004-02-07
期刊：
影响因子：
3.8
通讯作者：
Hamaguchi, M
中科院分区：
文献类型：
--
作者：
Iwamoto, T;Senga, T;Hamaguchi, M
M1小鼠白血病细胞在白细胞介素-6（IL-6）/白血病抑制因子（LIF）的刺激下分化为巨噬细胞/单核细胞。为了鉴定新的LIF诱导基因，我们使用M1细胞和克隆的小鼠白细胞介素-3（IL-3）受体β亚基基因进行了代表性差异分析。IL-3受体（IL-3R）α和β亚基的mRNA表达在LIF刺激1小时后上调，并且沿着M1细胞的分化保持升高。这种诱导在表达Stat 3显性阴性形式的M1细胞中几乎完全被抑制。此外，我们表明，IL-3诱导的员工磷酸化增加LIF刺激的M1细胞。这些结果表明，Stat 3可能通过调节IL-3R的表达在髓系细胞的分化中发挥作用。(C)2003 Elsevier Ltd.保留所有权利。
M1 mouse leukemia cells differentiate to macrophages/monocytes by the stimulation of interleukin-6 (IL-6)/leukemia inhibitory factor (LIF). To identify new LIF-induced genes, we have performed representational difference analysis using M1 cells and cloned mouse interleukin-3 (IL-3) receptor beta subunit gene. The mRNA expression of both IL-3 receptor (IL-3R) alpha and beta subunits is upregulated after 1 h stimulation of LIF and remains to be elevated along the differentiation of M1 cells. This induction is almost completely suppressed in M1 cells expressing a dominant negative form of Stat3. Furthermore, we show that IL-3-induced Staff phosphorylation increases in LIF-stimulated M 1 cells. These results suggest that Stat3 may play a role in the differentiation of myeloid cells by regulating IL-3R expression. (C) 2003 Elsevier Ltd. All rights reserved.