Induction of granulocytic differentiation in myeloblasts by 17-beta-estradiol involves the leukotriene D4 receptor.

Receptors & signal transduction Pub Date : 1996-01-01
V Dietsch, G F Kalf, B A Hazel
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引用次数: 0

Abstract

17-beta-Estradiol (beta E) causes granulocytic differentiation and neutrophilia in mice. However, the presence of estrogen receptors in myeloblasts and granulocytic progenitor cells has not been reported. beta E can be converted to a bioreactive species, estradiolquinone. We have previously shown that hydroquinone (HQ), via conversion to bioreactive p-benzoquinone (BQ), causes neutrophilia in mice and induces granulocytic differentiation in myeloblasts through interaction with the leukotriene D4 (LTD4) receptor. Therefore, we tested whether beta E could be oxidized by a myeloperoxidase-mediated reaction to a bioreactive intermediate, which might, in turn, induce granulocytic differentiation in mouse myeloblasts by activating the LTD4 receptor, thus obviating the need for LTD4, the downstream intracellular mediator of granulocyte colony-stimulating factor (G-CSF)-induced signal transduction. The interleukin (IL)-3-dependent, G-CSF-inducible normal mouse myeloblastic cell line, 32D cl 3(G), was used to determine the ability of beta E to induce terminal granulocytic differentiation in myeloblasts. Morphological analysis of stage-specific granulocytic differentiation indicated that beta E was capable of the concentration- (10(-8)-10(-4)M) and time-(6d) dependent induction of a complete program of terminal granulocytic differentiation in myeloblasts similar to that seen with G-CSF or LTD4. beta E-induced granulocytic differentiation was prevented by the peroxidase inhibitor, indomethacin, and was completely and competitively inhibited in the presence of a specific LTD4 receptor antagonist, MK-571, suggesting that a bioreactive form of estradiol, such as estradiolquinone, is interacting with the receptor. beta E was shown to cause a similar concentration-dependent induction of granulocytic differentiation in human HL-60 myeloblasts that was also inhibited by the receptor antagonist. Biological effects of beta E in nontarget tissues may result from the interaction of bioreactive estradiolquinone with critical cellular macromolecules involved in normal cellular signaling pathways.

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17- β -雌二醇诱导成髓细胞粒细胞分化涉及白三烯D4受体。
17- β -雌二醇(β E)引起小鼠粒细胞分化和嗜中性粒细胞增多。然而,雌激素受体在成髓细胞和粒细胞祖细胞中的存在尚未见报道。E可以转化为一种生物活性物质,雌二醇。我们之前已经证明,对苯二酚(HQ)通过转化为生物反应性对苯醌(BQ),导致小鼠中性粒细胞减少,并通过与白三烯D4 (LTD4)受体相互作用诱导成髓细胞的粒细胞分化。因此,我们测试了β E是否可以通过髓过氧化物酶介导的反应被氧化为一种生物反应中间体,这可能反过来通过激活LTD4受体诱导小鼠成髓细胞的粒细胞分化,从而消除了对LTD4的需求,LTD4是粒细胞集落刺激因子(G-CSF)诱导的信号转导的下游细胞内介质。利用白细胞介素(IL)-3依赖性、G- csf诱导的正常小鼠成髓细胞系32dcl3 (G)来测定β E诱导成髓细胞终粒分化的能力。阶段特异性粒细胞分化的形态学分析表明,β E能够以浓度依赖性(10(-8)-10(-4)M)和时间依赖性(6d)诱导成髓细胞的终末粒细胞分化,与G-CSF或LTD4类似。β e诱导的粒细胞分化被过氧化物酶抑制剂吲哚美辛阻止,并且在特异性LTD4受体拮抗剂MK-571的存在下被完全和竞争性地抑制,这表明雌二醇的生物反应形式,如雌二醇醌,与受体相互作用。β E在人HL-60成髓细胞中引起类似浓度依赖性的粒细胞分化诱导,也被受体拮抗剂抑制。β E在非靶组织中的生物学效应可能是由生物反应性雌二醇与参与正常细胞信号通路的关键细胞大分子相互作用引起的。
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