...
首页> 外文期刊>Cytokine >IL-1beta induces serine protease inhibitor 3 (SPI-3) gene expression in rat pancreatic beta-cells. Detection by differential display of messenger RNA.
【24h】

IL-1beta induces serine protease inhibitor 3 (SPI-3) gene expression in rat pancreatic beta-cells. Detection by differential display of messenger RNA.

机译:IL-1β诱导大鼠胰腺β细胞中丝氨酸蛋白酶抑制剂3(SPI-3)基因表达。通过差异显示信使RNA进行检测。

获取原文
获取原文并翻译 | 示例
           

摘要

Immune-mediated beta-cell damage induces diverse intracellular signals, leading to transcription of different genes which may either contribute to beta-cell repair and/or defence or lead to cell death. The cytokine interleukin-1beta (IL-1) is a potential mediator of beta-cell dysfunction and damage in type 1 diabetes mellitus. To understand the molecular actions of this cytokine upon beta-cells, this study aimed at the cloning of genes induced in FACS-purified rat pancreatic beta-cells by a 6- or 24-h exposure to IL-1 by using differential display of mRNA with reverse transcription-polymerase chain reaction (DDRT-PCR). Among these cytokine-induced genes, a gene encoding for rat serine protease inhibitor (SPI-3) was isolated. SPI-3 may be involved in cellular defence responses against inflammatory stress. RT-PCR analysis confirmed that SPI-3 mRNA expression in rat beta-cells is increased by IL-1 at an early stage (2 h), with maximal accumulation during 6-12 h and decline after 24 h. Similar observations were made in mouse pancreatic islets and in the rat insulinoma cell line RINm5F. IFN-gamma neither increased SPI-3 gene expression nor potentiated its induction by IL-1 in rat beta-cells. The stimulatory effects of IL-1 on SPI-3 mRNA expression were decreased by co-incubation with an inhibitor of gene transcription (actinomycin D), an inhibitor of protein synthesis (cycloheximide) or an inhibitor of NF-kappaB activation (PDTC). On the other hand, a blocker of inducible nitric oxide synthase (iNOS) activity (N(G)-methyl-L-arginine) did not prevent IL-1-induced SPI-3 expression. Thus, SPI-3 mRNA expression following IL-1 exposure depends on gene transcription, protein synthesis and activation of the nuclear transcription factor NF-kappaB, but it is independent of NO formation. Copyright 1999 Academic Press.
机译:免疫介导的β细胞损伤会诱导多种细胞内信号,导致不同基因的转录,而这些基因可能有助于β细胞修复和/或防御或导致细胞死亡。细胞因子白介素1β(IL-1)是1型糖尿病中β细胞功能障碍和损伤的潜在介质。为了了解该细胞因子对β细胞的分子作用,本研究旨在通过差异显示mRNA克隆通过FACS纯化的大鼠胰腺β细胞6或24小时暴露于IL-1诱导的基因克隆。逆转录聚合酶链反应(DDRT-PCR)。在这些细胞因子诱导的基因中,分离出编码大鼠丝氨酸蛋白酶抑制剂(SPI-3)的基因。 SPI-3可能参与针对炎症应激的细胞防御反应。 RT-PCR分析证实,大鼠β细胞中SPI-3 mRNA的表达在早期(2小时)被IL-1增加,在6-​​12小时内最大积累,在24小时后下降。在小鼠胰岛和大鼠胰岛素瘤细胞系RINm5F中也得到了类似的观察结果。 IFN-γ既不会增加SPI-3基因的表达,也不会增强IL-1在大鼠β细胞中的诱导作用。与基因转录抑制剂(放线菌素D),蛋白质合成抑制剂(环己酰亚胺)或NF-κB活化抑制剂(PDTC)共同孵育可降低IL-1对SPI-3 mRNA表达的刺激作用。另一方面,可诱导型一氧化氮合酶(iNOS)活性的阻滞剂(N(G)-甲基-L-精氨酸)不能阻止IL-1诱导的SPI-3表达。因此,IL-1暴露后SPI-3 mRNA的表达取决于基因转录,蛋白质合成和核转录因子NF-κB的激活,但与NO的形成无关。版权所有1999,学术出版社。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号