首页> 外文期刊>Physiological Research >Activation of Adenosine A(3) Receptors Potentiates Stimulatory Effects of IL-3, SCF, and GM-CSF on Mouse Granulocyte-Macrophage Hematopoietic Progenitor Cells
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Activation of Adenosine A(3) Receptors Potentiates Stimulatory Effects of IL-3, SCF, and GM-CSF on Mouse Granulocyte-Macrophage Hematopoietic Progenitor Cells

机译:腺苷A(3)受体的激活增强对小鼠粒细胞-巨噬细胞造血祖细胞的IL-3,SCF和GM-CSF的刺激作用。

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摘要

Adenosine A(3) receptor agonist N-6-(3-iodobenzyl)adenosine-5'-N-methyluronamide (IB-MECA) has been tested from the point of view of potentiating the effects of hematopoietic growth factors interleukin-3 (IL-3), stem cell factor (SCF), granulocyte-macrophage colony-stimulating factor (GM-CSF), and granulocyte colony-stimulating factor (G-CSF) on the growth of hematopoietic progenitor cells for granulocytes and macrophages (GM-CFC) in suspension of normal mouse bone marrow cells in vitro. IB-MECA alone induced no GM-CFC growth. Significant elevation of numbers of GM-CFC evoked by the combinations of IB-MECA with IL-3, SCF, or GM-CSF as compared with these growth factors alone has been noted. Combination of IB-MECA with G-CSF did not induce significantly higher numbers of GM-CFC in comparison with G-CSF alone. Joint action of three drugs, namely of IB-MECA + IL-3 + GM-CSF, produced significantly higher numbers of GM-CFC in comparison with the combinations of IB-MECA + IL-3, IB-MECA + GM- CSF, or IL-3 + GM-CSF. These results give evidence of a significant role of selective activation of adenosine A3 receptors in stimulation of the growth of granulocyte/macrophage hematopoietic progenitor cells.
机译:已从增强造血生长因子白介素3(IL)的作用角度测试了腺苷A(3)受体激动剂N-6-(3-碘苄基)腺苷5'-N-甲基脲酰胺(IB-MECA) -3),干细胞因子(SCF),粒细胞巨噬细胞集落刺激因子(GM-CSF)和粒细胞集落刺激因子(G-CSF)对粒细胞和巨噬细胞(GM-CFC)造血祖细胞的生长)悬浮于正常小鼠骨髓细胞中。仅IB-MECA不会引起GM-CFC的增长。与单独的这些生长因子相比,IB-MECA与IL-3,SCF或GM-CSF的组合引起的GM-CFC数量显着增加。与单独的G-CSF相比,IB-MECA与G-CSF的组合不会诱导明显更高数量的GM-CFC。与IB-MECA + IL-3,IB-MECA + GM-CSF的组合相比,三种药物(即IB-MECA + IL-3 + GM-CSF)的共同作用产生了更高数量的GM-CFC,或IL-3 + GM-CSF。这些结果提供了腺苷A3受体的选择性激活在刺激粒细胞/巨噬细胞造血祖细胞生长中的重要作用的证据。

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