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首页> 外文期刊>Molecular and Cellular Biology >The zinc finger transcription factor Egr-1 potentiates macrophage differentiation of hematopoietic cells.
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The zinc finger transcription factor Egr-1 potentiates macrophage differentiation of hematopoietic cells.

机译：锌指转录因子Egr-1增强造血细胞的巨噬细胞分化。

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Previously we have shown that the zinc finger transcription factor Egr-1 is essential for and restricts differentiation of hematopoietic cells along the macrophage lineage, raising the possibility that Egr-1 actually plays a deterministic role in governing the development of hematopoietic precursor cells along the monocytic lineage. To test this hypothesis, we have taken advantage of interleukin-3-dependent 32Dcl3 hematopoietic precursor cells which, in addition to undergoing granulocytic differentiation in response to granulocyte colony-stimulating factor, were found to be induced for limited proliferation, but not differentiation, by granulocyte-macrophage colony-stimulating factor. It was shown that ectopic expression of Egr-1 blocked granulocyte colony-stimulating factor-induced terminal granulocytic differentiation, consistent with previous findings. In addition, ectopic expression of Egr-1 endowed 32Dcl3 cells with ability to be induced by granulocyte-macrophage colony-stimulating factor for terminal differentiation exclusively along the macrophage lineage. Thus, evidence that Egr-1 potentiates terminal macrophage differentiation has been obtained, suggesting that Egr-1 plays a deterministic role in governing the development of hematopoietic cells along the macrophage lineage.
机译：先前我们已经表明锌指转录因子Egr-1对于沿巨噬细胞谱系的造血细胞分化至关重要，并限制了其分化，这增加了Egr-1实际上在控制沿单核细胞的造血前体细胞发育中发挥确定性作用的可能性血统。为了验证这一假设，我们利用了白介素3依赖性的32Dcl3造血前体细胞，该细胞除了响应粒细胞集落刺激因子而经历粒细胞分化外，还被诱导诱导了有限的增殖，但未诱导分化。粒细胞巨噬细胞集落刺激因子。结果表明，Egr-1的异位表达阻断了粒细胞集落刺激因子诱导的终末粒细胞分化，与以前的发现一致。另外，Egr-1的异位表达赋予了32Dcl3细胞以粒细胞-巨噬细胞集落刺激因子诱导的能力，使其仅沿巨噬细胞谱系终末分化。因此，已获得Egr-1增强终末巨噬细胞分化的证据，表明Egr-1在控制沿巨噬细胞谱系的造血细胞发育中起决定性作用。

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