Bristulf J, Gatti S, Malinowsky D, Bjork L, Sundgren A K, Bartfai T
Department of Neurochemistry and Neurotoxicology, Arrhenius Laboratories for Natural Sciences, Stockholm University, Sweden.
Eur Cytokine Netw. 1994 May-Jun;5(3):319-30.
The insulin secreting rat Rinm5F cells are often used to study the cytotoxic actions of interleukin-1 (IL-1) on pancreatic beta-cells. We demonstrate here that Rinm5F insulinoma cells express both type I and type II interleukin-1 receptor (IL-1R) mRNAs and gene products. IL-1R agonists, recombinant murine IL-1 alpha (rmIL-1 alpha, 10 ng/ml) and recombinant rat IL-1 beta (rrIL-1 beta, 100 pg/ml or 10 ng/ml) induce the upregulation of mRNA expression for both types of IL-1 receptors (IL-1Rs). This effect of rrIL-1 beta is antagonised by preincubation with recombinant human interleukin 1 receptor antagonist protein (rhIL-1ra, 5 micrograms/ml). Furthermore, this rrIL-1 beta induced upregulation of IL-1R mRNAs is blocked by actinomycin D (7.5 micrograms/ml), whereas cycloheximide (20 micrograms/ml) has no effect. The phorbol ester PMA (20 nM) upregulates the expression of mRNAs both IL-1 receptors, whereas glucose (50 mM) upregulates the expression of the type I IL-1R mRNA only. Pretreatment of cells with pertussis toxin (100 ng/ml) partially blocks the rrIL-1 beta induced expression of mRNA for the type I and, to a lesser extent, the type II IL-1R. Incubation of the cells with rrIL-1 beta also induces a time-dependent expression of c-fos, interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-alpha) mRNAs. Binding studies with 125I-recombinant human IL-1 beta (125I-rhIL-1 beta) indicate that IL-1R gene products, with the ligand binding characteristics of the type I IL-1R, are constitutively present on Rinm5F cells. Treatment with rrIL-1 beta (6h) increases the number of 125I-rhIL-1 beta binding sites on Rinm5F cells. We have also demonstrated that the number of type II IL-1R binding sites increases after induction with rrIL-1 beta (6h), by indirect immunofluorescence using a monoclonal antibody (ALVA 42) raised against the human type II IL-1R. Furthermore, we have sequenced the type II IL-1R cDNA in the rat insulinoma Rinm5F cells. The comparison of the amino acid sequence of the rat type II IL-1R with that of the mouse and human type II IL-1Rs shows 90% and 62% amino acid identity, respectively. The most important difference between the human and murine type II IL-1Rs, and this rat type II IL-1R cDNA, is an open reading frame coding for a six amino acid longer, strongly charged (QIKEMK), cytosolic domain.(ABSTRACT TRUNCATED AT 400 WORDS)
胰岛素分泌型大鼠Rinm5F细胞常被用于研究白细胞介素 -1(IL -1)对胰腺β细胞的细胞毒性作用。我们在此证明,Rinm5F胰岛素瘤细胞表达I型和II型白细胞介素 -1受体(IL -1R)的mRNA及基因产物。IL -1R激动剂,重组鼠IL -1α(rmIL -1α,10 ng/ml)和重组大鼠IL -1β(rrIL -1β,100 pg/ml或10 ng/ml)可诱导两种类型IL -1受体(IL -1Rs)的mRNA表达上调。rrIL -1β的这种作用可被与重组人白细胞介素1受体拮抗剂蛋白(rhIL -1ra,5微克/毫升)预孵育所拮抗。此外,rrIL -1β诱导的IL -1R mRNA上调被放线菌素D(7.5微克/毫升)阻断,而环己酰亚胺(20微克/毫升)则无作用。佛波酯PMA(20 nM)上调两种IL -1受体的mRNA表达,而葡萄糖(50 mM)仅上调I型IL -1R mRNA的表达。用百日咳毒素(100 ng/ml)预处理细胞可部分阻断rrIL -1β诱导的I型IL -1R mRNA表达,对II型IL -1R mRNA表达的阻断作用较小。用rrIL -1β孵育细胞还可诱导c -fos、白细胞介素 -6(IL -6)和肿瘤坏死因子α(TNF -α)mRNA的时间依赖性表达。用125I -重组人IL -1β(125I -rhIL -1β)进行的结合研究表明,具有I型IL -1R配体结合特性的IL -1R基因产物在Rinm5F细胞上组成性存在。用rrIL -1β处理(6小时)可增加Rinm5F细胞上125I -rhIL -1β结合位点的数量。我们还通过使用针对人II型IL -1R产生的单克隆抗体(ALVA 42)进行间接免疫荧光证明,用rrIL -1β诱导(6小时)后II型IL -1R结合位点的数量增加。此外,我们对大鼠胰岛素瘤Rinm5F细胞中的II型IL -1R cDNA进行了测序。大鼠II型IL -1R的氨基酸序列与小鼠和人II型IL -1Rs的氨基酸序列比较显示,分别具有90%和62%的氨基酸同一性。人与鼠II型IL -1Rs以及该大鼠II型IL -1R cDNA之间最重要的差异是一个开放阅读框,其编码的胞质结构域长六个氨基酸,带强电荷(QIKEMK)。(摘要截短于400字)