...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Modulation of PAI-1 and proMMP-9 syntheses by soluble TNFalpha and its receptors during differentiation of the human monocytic HL-60 cell line.
【24h】

Modulation of PAI-1 and proMMP-9 syntheses by soluble TNFalpha and its receptors during differentiation of the human monocytic HL-60 cell line.

机译：调制PAI-1和proMMP-9合成可溶性TNFalpha及其受体在人类单核细胞的分化HL-60细胞线。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

During phorbol ester-induced differentiation of HL-60 monocytic cells, tumor necrosis factoralpha (TNFalpha) synthesis and secretion are increased, which contributes to the autocrine regulation of TNFalpha-responsive genes. We investigated how, during phorbol ester-induced differentiation of HL-60 cells, the secreted TNFalpha modulated plasminogen activator inhibitor type I (PAI-1) and gelatinase B (MMP-9) syntheses, two proteins involved in pericellular proteolysis. The differentiation-induced release of TNFalpha, was abolished by the hydroxamate-based matrix metalloproteinase (MMP) inhibitor, RU36156. RU36156 or a neutralizing anti-TNFalpha significantly down-regulated PAI-1 synthesis exclusively during the early phases of differentiation (from promyelocyte to monocytic-like cells), which underlined the activating role of autocrine TNFalpha during this time range. As cells progressed to monocyte/macrophage phenotype, they still released TNFalpha, but RU36156 or anti-TNFalpha no longer had an effect on PAI-1 synthesis. This lack of effect was not due to a default of TNFalpha signaling since PAI-1 synthesis was still stimulated in response to exogenous TNFalpha. TNFalpha receptor RI was also actively released and was shown to reduce TNFalpha activity which may account for the inability of soluble TNFalpha to up-regulate PAI-1 synthesis. In later mature stage, cells became susceptible to exogenous TNFalpha-induced apoptosis and rapidly lost their ability to respond to TNFalpha. The MMP-9 synthesis followed similar regulation as PAI-1. Isolated human blood monocytes-derived macrophages behave like HL-60-derived macrophages. In conclusion, these results show that during leukocyte differentiation, time windows exist during which the autocrine TNFalpha is active and then down-regulated by RI, which may temper a continuous up-regulation of the synthesis of proteins involved in pericellular proteolysis. J. Cell. Physiol. 196: 346-353, 2003.
机译：在佛波醇ester-induced分化HL-60单核细胞的细胞,肿瘤坏死factoralpha(TNFalpha)合成和分泌增加,导致的自分泌调节TNFalpha-responsive基因。在佛波醇ester-induced分化HL-60细胞,分泌TNFalpha调制纤溶酶原激活物抑制剂1型(PAI-1)白明胶酶B (MMP-9)合成两种蛋白质参与pericellular蛋白水解作用。TNFalpha differentiation-induced释放的被hydroxamate-based矩阵金属蛋白酶(MMP)抑制剂,RU36156。RU36156或中和anti-TNFalpha显著抑制PAI-1合成只在早期阶段(从早幼粒细胞分化monocytic-like细胞),强调了激活的角色自分泌TNFalpha在这时间范围。单核细胞/巨噬细胞表型,他们仍然TNFalpha公布,但RU36156或anti-TNFalpha不再有影响PAI-1合成。缺乏效果并不是由于违约自PAI-1 TNFalpha信号合成仍在对外源性刺激TNFalpha。发布,并可以减少TNFalpha活动可能占的无能可溶性TNFalpha会上调PAI-1合成。在后来的成熟阶段,细胞变得敏感外生TNFalpha-induced凋亡和迅速失去反应能力TNFalpha。PAI-1监管。monocytes-derived巨噬细胞像HL-60-derived巨噬细胞。结果表明,在白细胞分化、时间窗口中存在然后自分泌TNFalpha活跃由国际扶轮衰减,可能脾气连续上调的合成蛋白质参与pericellular蛋白水解作用。细胞。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号