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血小板活化因子诱导未分化及分化的U937细胞中肌醇1,4,5-三磷酸的生成:酪氨酸激酶的作用

Platelet-activating factor-induced inositol 1,4,5-trisphosphate generation in undifferentiated and differentiated U937 cells: role of tyrosine kinase.

作者信息

Abebe W, Ali N, Agrawal D K

机构信息

Allergic Disease Center, Creighton University School of Medicine, Omaha, NE 68178, USA.

出版信息

Int J Immunopharmacol. 1996 Mar;18(3):173-81. doi: 10.1016/0192-0561(96)00004-5.

DOI:10.1016/0192-0561(96)00004-5
PMID:8796445
Abstract

We compared the effect of platelet-activating factor (PAF) on inositol 1,4,5-trisphosphate (IP3) content in undifferentiated and differentiated U937 cells. In both cell types, PAF induced a rapid transient and concentration-dependent elevation of IP3 content. The production of IP3 in response to PAF was greater in differentiated than in undifferentiated cells. The increases in IP3 produced by PAF in both types of cell were inhibited by the PAF receptor antagonist, WEB 2086, as well as by the tyrosine kinase inhibitor, genistein. PAF also caused increased tyrosine phosphorylation of a 32 kDa protein substrate in both undifferentiated and differentiated cells. The magnitude of the phosphorylation was, however, greater in the differentiated cells. Genistein reduced the PAF-induced tyrosine phosphorylation of the substrate in both cell preparations. The specific binding of [3H]PAF was also markedly enhanced in differentiated cells. This effect was attenuated by genistein. The results indicate that PAF induces the production of IP3 in U937 cells via tyrosine kinase-mediated mechanisms and this process is augmented in differentiated cells.

摘要

我们比较了血小板活化因子(PAF)对未分化和分化的U937细胞中肌醇1,4,5 - 三磷酸(IP3)含量的影响。在这两种细胞类型中,PAF均诱导IP3含量迅速短暂且浓度依赖性升高。与未分化细胞相比,分化细胞中PAF诱导产生的IP3更多。PAF在这两种细胞类型中所引起的IP3增加均受到PAF受体拮抗剂WEB 2086以及酪氨酸激酶抑制剂染料木黄酮的抑制。PAF还导致未分化和分化细胞中一种32 kDa蛋白质底物的酪氨酸磷酸化增加。然而,分化细胞中磷酸化的程度更大。染料木黄酮降低了两种细胞制剂中PAF诱导的底物酪氨酸磷酸化。[3H]PAF的特异性结合在分化细胞中也显著增强。这种效应被染料木黄酮减弱。结果表明,PAF通过酪氨酸激酶介导的机制诱导U937细胞中IP3的产生,并且这一过程在分化细胞中增强。

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