Erythropoietin causes down regulation of colony-stimulating factor (CSF-1) receptors on peritoneal exudate macrophages of the mouse.

Erythropoietin causes down regulation of colony-stimulating factor (CSF-1) receptors on peritoneal exudate macrophages of the mouse.
复制标题

促红细胞生成素导致小鼠腹膜渗出巨噬细胞上的集落刺激因子 (CSF-1) 受体下调。

DOI:
10.1083/jcb.97.6.1945
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发表时间:
1983-12
期刊:
The Journal of cell biology
影响因子:
--
通讯作者:
Chen BD
Chen BD
中科院分区:
其他
文献类型:
--
作者:
Van Zant G;Chen BD

文献摘要

被引文献

相似文献

我们已经表明红细胞生成素(epo)(红细胞形成的主要调节剂)减少了主要巨噬细胞生长调节剂集落刺激因子(CSF-1)与腹膜渗出物巨噬细胞(PEM)的结合。epo对125 I-CSF-1结合的影响是剂量依赖性的;在1-2 U epo/ml(10(-10)M)的浓度下,CSF- 1结合几乎被完全抑制。促红细胞生成素不与CSF-1竞争后者受体的占用。epo对CSF-1结合的影响发生在37 ℃,而不是2 ℃,并且在PEM在37 ℃连续暴露于epo期间,我们发现CSF-1结合在1小时达到最低点,并在7小时内恢复到暴露前的水平.我们的新的结果是一致的概念,即EPO的特异性受体存在于PEM的细胞表面上,并且EPO的结合启动了一系列导致CSF-1受体内化的细胞事件。因此,epo引起PEM上CSF-1受体的下调。我们以前已经表明,促红细胞生成素导致抑制CSF诱导的小鼠骨髓细胞的粒细胞-巨噬细胞集落形成。我们在这里提出的结果提供了一个可能的机制,这些结果。
We have shown that erythropoietin (epo), the primary regulator of erythrocyte formation, diminished the binding to peritoneal exudate macrophages (PEM) of the principal macrophage growth regulator, colony- stimulating factor (CSF-1). The effect of epo on 125I-CSF-1 binding was dose-dependent; at a concentration of 1-2 U of epo/ml (10(-10) M), CSF- 1 binding was almost completely suppressed. Erythropoietin did not compete with CSF-1 for occupancy of the latter's receptors. The effect of epo on CSF-1 binding occurred at 37 degrees C but not at 2 degrees C, and during the continuous exposure of PEM to epo at 37 degrees C we found that CSF-1 binding reached a nadir at 1 h and recovered to pre- exposure levels in 7 h. Our novel results are consistent with the notion that specific receptors for epo exist on the cell surface of PEM and that binding of epo sets in motion a series of cellular events resulting in the internalization of CSF-1 receptors. Thus epo causes down regulation of CSF-1 receptors on PEM. We have previously shown that epo causes suppression of CSF-induced granulocyte-macrophage colony formation by mouse bone marrow cells. The results we present here provide a possible mechanism for these results.