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激动剂诱导人单核细胞中血小板活化因子受体信使核糖核酸的上调。

Agonist-induced up-regulation of platelet-activating factor receptor messenger RNA in human monocytes.

作者信息

Shirasaki H, Adcock I M, Kwon O J, Nishikawa M, Mak J C, Barnes P J

机构信息

Department of Thoracic Medicine, National Heart and Lung Institute, London, UK.

出版信息

Eur J Pharmacol. 1994 Jul 15;268(2):263-6. doi: 10.1016/0922-4106(94)90197-x.

Abstract

Platelet-activating factor (PAF) is a potent inflammatory mediator and it actions are mediated via specific cell surface receptors which are coupled to G-proteins. PAF stimulates several functions in monocytes and may modulate the expression of its own receptor. To investigate the possible modulation of PAF receptor mRNA expression Northern blot analysis of total RNA from human monocytes was performed using the cDNA of human leukocyte PAF receptor as a probe. Following the addition of 100 nM PAF, there was a 2.0-fold increase in PAF receptor mRNA at 60 minutes after the stimulation, which was inhibited by pretreatment with the PAF receptor antagonist WEB 2086. This increase returned to control level at 120 and 180 min. The increase of PAF receptor mRNA was statistically significant for 10 nM to 1 microM of PAF, while 100 nM of lysoPAF did not increase PAF receptor mRNA levels. These results suggest that PAF receptor expression can be regulated by PAF itself at the transcriptional level.

摘要

血小板活化因子(PAF)是一种强效炎症介质,其作用通过与G蛋白偶联的特定细胞表面受体介导。PAF刺激单核细胞的多种功能,并可能调节其自身受体的表达。为了研究PAF受体mRNA表达的可能调节,使用人白细胞PAF受体的cDNA作为探针,对人单核细胞的总RNA进行Northern印迹分析。加入100 nM PAF后,刺激后60分钟PAF受体mRNA增加了2.0倍,这被PAF受体拮抗剂WEB 2086预处理所抑制。这种增加在120和180分钟时恢复到对照水平。对于10 nM至1 μM的PAF,PAF受体mRNA的增加具有统计学意义,而100 nM的溶血PAF并未增加PAF受体mRNA水平。这些结果表明,PAF受体表达可在转录水平上由PAF自身调节。

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