All-trans retinoic acid upregulates thrombomodulin and downregulates tissue-factor expression in acute promyelocytic leukemia cells: distinct expression of thrombomodulin and tissue factor in human leukemic cells.

All-trans retinoic acid upregulates thrombomodulin and downregulates tissue-factor expression in acute promyelocytic leukemia cells: distinct expression of thrombomodulin and tissue factor in human leukemic cells.
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全反式视黄酸上调急性早幼粒细胞白血病细胞中血栓调节蛋白并下调组织因子表达:人类白血病细胞中血栓调节蛋白和组织因子的不同表达。

DOI:
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发表时间:
1994
期刊:
影响因子:
20.3
通讯作者:
N. Aoki
N. Aoki
中科院分区:
医学1区
文献类型:
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作者:
T. Koyama;S. Hirosawa;N. Kawamata;S. Tohda;N. Aoki

文献摘要

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本文研究了全反式维甲酸(ATRA)对人白血病细胞株NB4(急性早幼粒细胞白血病)和U937(单核细胞白血病)血栓调节蛋白(TM)和组织因子(TF)表达的影响。ATRA显着上调TM抗原在细胞裂解物中的表达,以及TM辅因子活性的NB4细胞表面上。ATRA可增加NB 4细胞中TM mRNA的水平。NB4细胞固有的促凝血因子含量明显增高,ATRA可有效降低其含量。当用二丁酰环磷酸腺苷(dbcAMP)处理NB 4细胞时,观察到TM适度增加,TF减少。ATRA和dbcAMP均能显著提高U937细胞TM抗原水平,而TF抗原水平则略有下降。这些结果表明,ATRA调节NB 4和U937细胞系中TM和TF抗原的表达和活性,并为ATRA作为早幼粒细胞和单核细胞白血病弥散性血管内凝血的预防和治疗剂的潜在有效性提供了证据。
The expressions of thrombomodulin (TM) and tissue factor (TF) by all-trans retinoic acid (ATRA) were studied in human leukemic cell lines including NB4 (acute promyelocytic leukemia) and U937 (monoblastic leukemia). ATRA remarkably upregulated TM antigen expression in cell lysates as well as TM cofactor activity on the cell surfaces of NB4. The level of TM mRNA in NB4 cells was increased by ATRA. Inherently procoagulant NB4 cells contained markedly higher content of TF, which was efficiently reduced by ATRA. Modest increase of TM and decrease of TF were observed when NB4 cells were treated with dibutyryl cyclic adenosine monophosphate (dbcAMP). On the other hand, both ATRA and dbcAMP showed dramatic increase of TM antigen level and modest decrease of TF antigen in U937 cells. These results suggest that ATRA regulates expressions of TM and TF antigens and activity in NB4 and U937 cell lines, and provide evidence for a potential efficiency of ATRA as a preventive and therapeutic agent for disseminated intravascular coagulation in promyelocytic and monocytic leukemia.