白血病抑制因子刺激的M1小鼠白血病细胞中Stat3依赖性白细胞介素-3受体表达的诱导

Stat3-dependent induction of interleukin-3 receptor expression in leukemia inhibitory factor-stimulated M1 mouse leukemia cells.

作者信息

Iwamoto Takashi, Senga Takeshi, Adachi Koichi, Hamaguchi Michinari

机构信息

Radioisotope Research Center Medical Division, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan.

出版信息

Cytokine. 2004 Feb 7;25(3):136-9. doi: 10.1016/j.cyto.2003.10.009.

DOI:10.1016/j.cyto.2003.10.009

PMID:14698140

Abstract

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 Stat5 phosphorylation increases in LIF-stimulated M1 cells. These results suggest that Stat3 may play a role in the differentiation of myeloid cells by regulating IL-3R expression.

摘要

M1小鼠白血病细胞通过白细胞介素-6（IL-6）/白血病抑制因子（LIF）的刺激分化为巨噬细胞/单核细胞。为了鉴定新的LIF诱导基因，我们使用M1细胞进行了代表性差异分析，并克隆了小鼠白细胞介素-3（IL-3）受体β亚基基因。在LIF刺激1小时后，IL-3受体（IL-3R）α和β亚基的mRNA表达均上调，并在M1细胞分化过程中持续升高。在表达显性负性形式Stat3的M1细胞中，这种诱导几乎被完全抑制。此外，我们表明在LIF刺激的M1细胞中，IL-3诱导的Stat5磷酸化增加。这些结果表明，Stat3可能通过调节IL-3R表达在髓系细胞分化中发挥作用。