MYELOID CELL-PROLIFERATION STIMULATED BY STEEL FACTOR IS PERTUSSIS-TOXIN-SENSITIVE AND ENHANCED BY CHOLERA-TOXIN
MYELOID CELL-PROLIFERATION STIMULATED BY STEEL FACTOR IS PERTUSSIS-TOXIN-SENSITIVE AND ENHANCED BY CHOLERA-TOXIN
复制标题
DOI：
10.1016/0192-0561(94)90106-6
复制
发表时间：
1994-07-01
期刊：
影响因子：
--
通讯作者：
BROXMEYER, HE
中科院分区：
文献类型：
--
作者：
HENDRIE, PC;BROXMEYER, HE
本文研究了G蛋白毒素对钢铁因子（SLF）和粒细胞-巨噬细胞集落刺激因子（GM-CSF）刺激人因子依赖细胞系M07 e增殖的影响。百日咳毒素预处理抑制GM-CSF或Steel因子诱导的增殖54 +/-8%;然而，GM-CSF + Steel因子联合诱导的增殖抑制程度要小得多（14 +/-8%）。用霍乱毒素预处理M07 e细胞，分别抑制GM-CSF和GM-CSF加Steel因子刺激的增殖57 +/-6%和79%，但单独对Steel因子的增殖反应增加两倍。观察到百日咳毒素和霍乱毒素对人脐带血正常髓系祖细胞增殖的类似作用。百日咳毒素处理M07 e细胞4小时导致40 - 42 kDa蛋白条带的ADP-核糖基化，但没有显著增加环AMP水平。霍乱毒素预处理与细胞内环磷酸腺苷水平增加10倍相关。这些结果暗示了GM-CSF和Steel因子两者的百日咳毒素敏感途径，但表明这些途径可能不是由组合刺激的协同增殖所需的。此外，由GM-CSF（一种Steel因子）刺激的增殖对霍乱毒素预处理敏感;而霍乱毒素预处理增强了由Steel因子刺激的增殖，可能是通过增加环AMP。这表明两种细胞因子的不同信号转导途径。
Effects of G-protein toxins on Steel factor (SLF) and granulocyte-macrophage colony stimulating factor (GM-CSF) stimulated proliferation of human factor-dependent cell line, M07e, were evaluated. Pertussis toxin pretreatment suppressed GM-CSF- or Steel factor-induced proliferation by 54 +/- 8%; however, proliferation induced by the combination of GM-CSF plus Steel factor was suppressed to a much lesser extent (14 +/- 8%). Pretreatment of M07e cells with cholera toxin, suppressed GM-CSF- and GM-CSF plus Steel factor-stimulated proliferation by 57 +/- 6% and 79%, respectively, but increased the proliferative response to Steel factor alone by twofold. Similar effects of pertussis toxin and cholera toxin were observed on proliferation of normal myeloid progenitor cells from human umbilical cord blood. Pertussis toxin treatment of M07e cells for 4 h resulted in the ADP-ribosylation of 40 - 42 kDa protein band but did not significantly increase cyclic AMP levels. Cholera toxin pretreatment was associated with a 10-fold increase in intracellular cyclic AMP levels. These results implicate pertussis toxin sensitive pathways for both GM-CSF and Steel factor, but suggest that these pathways may not be required for synergistic proliferation stimulated by the combination. In addition, proliferation stimulated by GM-CSF, a Steel factor, is sensitive to cholera toxin pretreatment; whereas cholera toxin pretreatment enhanced proliferation stimulated by Steel factor, possibly via increased cyclic AMP. This suggests divergent signal transduction pathways for the two cytokines.