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一种与I型白细胞介素-1受体同源的信使核糖核酸在培养的大鼠交感神经节中表达。

An mRNA homologous to interleukin-1 receptor type I is expressed in cultured rat sympathetic ganglia.

作者信息

Hart R P, Liu C, Shadiack A M, McCormack R J, Jonakait G M

机构信息

Department of Biological Sciences, Rutgers University, Newark, NJ 07102.

出版信息

J Neuroimmunol. 1993 Apr;44(1):49-56. doi: 10.1016/0165-5728(93)90267-3.

DOI:10.1016/0165-5728(93)90267-3
PMID:7684399
Abstract

Interleukin-1 (IL-1) induces substance P (SP) gene expression in cultured rat superior cervical ganglion (SCG) explants. In order to study the molecular mechanism of this action of IL-1, the presence of an interleukin-1 receptor (IL-1R) activity and the identity of an mRNA homologous to known IL-1R sequence was determined in SCG. The SP increase is blocked by recombinant IL-1 receptor antagonist protein, so IL-1 must be interacting with a specific receptor. We have cloned cDNA homologous to IL-1R type I from rat SCG using a reverse transcription-polymerase chain reaction (RT-PCR). The resulting cDNA sequence is strongly homologous with mouse and human IL-1R cDNA of the T cell and fibroblast type (type I; encoding an 80-kDa protein). mRNA specific for IL-1R can be readily detected in intact SCG by quantitative RT-PCR and S1 hybridization. However, the level of IL-1R mRNA increases 3-6-fold by 2 days in culture. This increase is independent of the presence of dexamethasone, IL-1 beta or IL-1 receptor antagonist protein ligands. The increase of IL-1R following explantation, a model of nerve injury, may provide a mechanism linking inflammatory signalling to neuronal phenotypic changes.

摘要

白细胞介素-1(IL-1)可诱导培养的大鼠颈上神经节(SCG)外植体中P物质(SP)基因的表达。为了研究IL-1这一作用的分子机制,我们检测了SCG中白细胞介素-1受体(IL-1R)活性的存在情况以及与已知IL-1R序列同源的mRNA的特性。SP的增加可被重组IL-1受体拮抗剂蛋白阻断,因此IL-1必定是与一种特异性受体相互作用。我们利用逆转录-聚合酶链反应(RT-PCR)从大鼠SCG中克隆了与I型IL-1R同源的cDNA。所得的cDNA序列与T细胞和成纤维细胞类型(I型;编码一种80 kDa的蛋白质)的小鼠和人IL-1R cDNA高度同源。通过定量RT-PCR和S1杂交可在完整的SCG中轻易检测到IL-1R特异性的mRNA。然而,培养2天后IL-1R mRNA水平增加3至6倍。这种增加与地塞米松、IL-1β或IL-1受体拮抗剂蛋白配体的存在无关。在外植(一种神经损伤模型)后IL-1R的增加可能提供了一种将炎症信号与神经元表型变化联系起来的机制。

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