Suppr超能文献

功能性人集落刺激因子-1受体在小鼠骨髓红系祖细胞上的表达。

Expression of functional human CSF-1 receptors on mouse bone marrow erythroid progenitor cells.

作者信息

Mouchiroud G, Bourette R, Blanchet J P

机构信息

Centre de Génétique Moléculaire et Cellulaire, UMR CNRS 106, Université Claude-Bernard, Villeurbanne, France.

出版信息

C R Acad Sci III. 1993 Nov;316(11):1290-6.

PMID:8087610
Abstract

We have previously shown that a murine multipotent hematopoietic cell line could proliferate in response to CSF-1 after retroviral transfer of human CSF-1 receptor (CSF-1R) gene (c-fms) without loss of the erythroid differentiation potential. In the light of these data, we asked whether ectopic expression of human c-fms gene would lead to the conditional immortalization of murine hematopoietic progenitor cells. In the present studies, murine bone marrow cells were infected with recombinant retroviruses containing the human c-fms cDNA. We found that CSF-1 could exert a stimulatory activity on erythroid progenitors in the presence of Epo only when bone marrow cells had been previously infected with c-fms retroviruses. In addition, expression of human CSF-1R in murine Epo-dependent, v-src-immortalized cells resulted in CSF-1-dependent proliferation of these cells in the absence of Epo. These data show that human CSF-1R (i) can stimulate early bone marrow erythroid progenitors, (ii) might require additional signals provided by oncogenes or cytokine receptors to transduce a mitogenic signal into mouse bone marrow erythroid progenitors.

摘要

我们之前已经表明,在逆转录病毒转导人集落刺激因子-1受体(CSF-1R)基因(c-fms)后,一种小鼠多能造血细胞系能够对CSF-1作出增殖反应,且不丧失红系分化潜能。鉴于这些数据,我们询问人c-fms基因的异位表达是否会导致小鼠造血祖细胞的条件性永生化。在本研究中,用含有人类c-fms cDNA的重组逆转录病毒感染小鼠骨髓细胞。我们发现,只有当骨髓细胞先前已被c-fms逆转录病毒感染时,CSF-1才能够在促红细胞生成素(Epo)存在的情况下对红系祖细胞发挥刺激活性。此外,在小鼠依赖Epo的、v-src永生化细胞中表达人CSF-1R导致这些细胞在没有Epo的情况下依赖CSF-1增殖。这些数据表明,人CSF-1R(i)能够刺激早期骨髓红系祖细胞,(ii)可能需要癌基因或细胞因子受体提供的额外信号,才能将促有丝分裂信号转导至小鼠骨髓红系祖细胞。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验