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人巨核母细胞系UT-7中血栓调节蛋白的生物合成及其被二丁酰环磷腺苷增强的作用

The biosynthesis of thrombomodulin and its enhancement by dibutyryl cAMP in a human megakaryoblastic cell line, UT-7.

作者信息

Ohashi K, Hirokawa K, Komatsu N, Aoki N

机构信息

First Department of Internal Medicine, Tokyo Medical and Dental University, Japan.

出版信息

Int J Hematol. 1991 Aug;54(4):341-9.

PMID:1663800
Abstract

Thrombomodulin (TM) is an endothelial cell membrane glycoprotein which modulates coagulation via the formation of thrombin-TM complexes. We investigated the human megakaryoblastic cell line (UT-7) for the presence of functional TM on the cell surface and in cell lysates using a specific enzyme-linked immunosorbent assay, a functional assay, and analysis by fluorescent activated cell sorter. We also examined the effect of cyclic nucleotides on TM in UT-7 cells. Quiescent UT-7 cells contained TM protein in cell lysates, but no TM antigen was observed on the cell surface. Dibutyryl cyclic AMP up-regulated TM: UT-7 cells transiently expressed functional TM antigen on the cell surface via de novo synthesis of TM protein resulting from increased TM mRNA levels. In contrast, dibutyryl cyclic GMP did not significantly affect TM antigen levels. The results suggest that megakaryocytes produce TM antigen and protein kinase A are involved in cellular mechanisms of TM expression.

摘要

血栓调节蛋白(TM)是一种内皮细胞膜糖蛋白,它通过形成凝血酶 - TM复合物来调节凝血。我们使用特异性酶联免疫吸附测定、功能测定以及荧光激活细胞分选仪分析,研究了人巨核母细胞系(UT - 7)细胞表面和细胞裂解物中功能性TM的存在情况。我们还研究了环核苷酸对UT - 7细胞中TM的影响。静止的UT - 7细胞在细胞裂解物中含有TM蛋白,但在细胞表面未观察到TM抗原。二丁酰环磷腺苷上调了TM:UT - 7细胞通过TM mRNA水平升高导致的TM蛋白从头合成,在细胞表面短暂表达功能性TM抗原。相比之下,二丁酰环磷鸟苷对TM抗原水平没有显著影响。结果表明巨核细胞产生TM抗原,蛋白激酶A参与TM表达的细胞机制。

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Int J Hematol. 1991 Aug;54(4):341-9.
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