DMSO reduces CSF-1 receptor levels and causes apoptosis in v-myc immortalized mouse macrophages
DMSO reduces CSF-1 receptor levels and causes apoptosis in v-myc immortalized mouse macrophages
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DOI：
10.1006/excr.1998.4149
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发表时间：
1998-08-25
影响因子：
3.7
通讯作者：
Righi, M
中科院分区：
文献类型：
--
作者：
Marthyn, P;Beuscart, A;Righi, M
由于 DMSO 对骨髓细胞产生细胞毒性作用，我们研究了二甲亚砜 (DMSO) 对 v-myc 永生化小鼠巨噬细胞的抗增殖潜力。 DMSO 在两种持续分泌集落刺激因子 1 (CSF-1) 的永生化巨噬细胞系中引起显着的细胞凋亡。与小鼠红白血病细胞的结果相反，DMSO 没有显着降低 Spi-1/PU.1 转录因子的水平。然而，与 Fc γ RIIIA 免疫球蛋白受体、v-myc 和 β-肌动蛋白相比，DMSO 导致 CSF-1 受体 (CSF-1R) 的蛋白水平特异性降低。为了研究 CSF-1R 的水平是否可能与 DMSO 诱导的细胞死亡呈负相关，我们衍生了可以在 DMSO 存在下培养的巨噬细胞培养物（称为 DN-11）。对使用或不使用 DMSO 生长的 DN-11 进行免疫印迹分析，结果显示在两种条件下均存在大量 CSF-1R，表明 CSF-1R 在 DMSO 处理的巨噬细胞的存活中发挥着关键作用。因此，在这些细胞中，DMSO 似乎通过中断涉及 CSF-1 受体的自分泌生存循环来触发细胞凋亡。 (C) 1998 年学术出版社。
We have investigated the antiproliferative potential of dimethyl sulfoxide (DMSO) on v-myc immortalized mouse macrophages on account of the cytotoxic effect induced by DMSO on myeloid cells. DMSO caused significant apoptosis in two immortalized macrophage cell lines constitutively secreting colony-stimulating factor 1 (CSF-1). In contrast to the results described for mouse erythroleukemia cells, DMSO did not markedly decrease the level of the Spi-1/PU.1 transcription factor. However, DMSO caused a specific reduction in the protein level of the CSF-1 receptor (CSF-1R) compared to the Fc gamma RIIIA immunoglobulin receptor, v-myc, and beta-actin proteins. To investigate if the level of CSF-1R might inversely correlate with DMSO-induced cell death, we derived a macrophage culture (named DN-11) that could be cultured in the presence of DMSO. Immunoblot analysis of DN-11, grown with or without DMSO, revealed significant amounts of CSF-1R under both conditions, suggesting a pivotal role for CSF-1R in the survival of DMSO-treated macrophages. Therefore, in these cells, DMSO seems to trigger apoptosis by interrupting an autocrine survival loop involving the CSF-1 receptor. (C) 1998 Academic Press.