Activated protein C suppresses tissue factor expression on U937 cells in the endothelial protein C receptor-dependent manner
Activated protein C suppresses tissue factor expression on U937 cells in the endothelial protein C receptor-dependent manner
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DOI：
10.1016/s0014-5793(00)01740-3
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发表时间：
2000-07-21
期刊：
影响因子：
3.5
通讯作者：
Terao, T
中科院分区：
文献类型：
--
作者：
Shu, F;Kobayashi, H;Terao, T
用培养的人单核细胞白血病U937细胞系研究了活化蛋白C（APC）在调节组织因子（TF）表达中的新功能。流式细胞荧光分析表明，APC治疗导致TF表达在未刺激和佛波酯刺激的细胞中的时间和剂量依赖性降低。内皮蛋白C/APC受体（EPCR）的单克隆抗体（mAb）252强烈抑制APC和EPCR之间的相互作用，而与EPCR结合而不阻断APC结合的mAb 49和379没有或仅具有适度的作用。结论是，在APC存在下培养U937细胞通过EPCR依赖性机制引起TF表达的下调，与诱导是否由佛波酯触发无关，（C）2000欧洲生物化学学会联合会。由Elsevier Science B. V.出版，版权所有。
The new functional role of activated protein C (APC) in the regulation of tissue factor (TF) expression was investigated using the cultured human monoblastic leukemia U937 cell line. A flow cytofluorometric analysis demonstrated that treatment with APC resulted in time- and dose-dependent decrease in TF expression in unstimulated and phorbol ester-stimulated cells. The effect was antagonized by the monoclonal antibody (mAb) to endothelial protein C/APC receptor (EPCR), 252, which strongly inhibited the interaction between APC and EPCR, In contrast, mAbs 49 and 379, which bind to EPCR without blocking APC binding, had no or only a modest effect. It is concluded that culturing U937 cells in the presence of APC caused down-regulation of TF expression through the EPCR-dependent mechanism, independent of whether induction was triggered by phorbol ester, (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.