Suppr超能文献

TLR 刺激后 THP1 衍生巨噬细胞中 TRIM 蛋白家族的表达谱分析。

Expression profiling of TRIM protein family in THP1-derived macrophages following TLR stimulation.

机构信息

Institute of Translational Medicine, Nanchang University, Nanchang, Jiangxi, 330031, China.

Department of Basic Medical Science, Shock/Trauma Research Center, School of Medicine, University of Missouri Kansas City, Kansas City, MO, 64108, USA.

出版信息

Sci Rep. 2017 Feb 17;7:42781. doi: 10.1038/srep42781.

Abstract

Activated macrophages play an important role in many inflammatory diseases including septic shock and atherosclerosis. However, the molecular mechanisms limiting macrophage activation are not completely understood. Members of the tripartite motif (TRIM) family have recently emerged as important players in innate immunity and antivirus. Here, we systematically analyzed mRNA expressions of representative TRIM molecules in human THP1-derived macrophages activated by different toll-like receptor (TLR) ligands. Twenty-nine TRIM members were highly induced (>3 fold) by one or more TLR ligands, among which 19 of them belong to TRIM C-IV subgroup. Besides TRIM21, TRIM22 and TRIM38 were shown to be upregulated by TLR3 and TLR4 ligands as previous reported, we identified a novel group of TRIM genes (TRIM14, 15, 31, 34, 43, 48, 49, 51 and 61) that were significantly up-regulated by TLR3 and TLR4 ligands. In contrast, the expression of TRIM59 was down-regulated by TLR3 and TLR4 ligands in both human and mouse macrophages. The alternations of the TRIM proteins were confirmed by Western blot. Finally, overexpression of TRIM59 significantly suppressed LPS-induced macrophage activation, whereas siRNA-mediated knockdown of TRIM59 enhanced LPS-induced macrophage activation. Taken together, the study provided an insight into the TLR ligands-induced expressions of TRIM family in macrophages.

摘要

活化的巨噬细胞在许多炎症性疾病中发挥重要作用,包括败血症休克和动脉粥样硬化。然而,限制巨噬细胞激活的分子机制尚不完全清楚。三部分基序 (TRIM) 家族成员最近已成为天然免疫和抗病毒的重要参与者。在这里,我们系统地分析了不同 Toll 样受体 (TLR) 配体激活的人 THP1 衍生巨噬细胞中代表性 TRIM 分子的 mRNA 表达。29 个 TRIM 成员被一种或多种 TLR 配体高度诱导 (>3 倍),其中 19 个属于 TRIM C-IV 亚组。除了之前报道的 TRIM21、TRIM22 和 TRIM38 被 TLR3 和 TLR4 配体上调外,我们还鉴定了一组新的 TRIM 基因 (TRIM14、15、31、34、43、48、49、51 和 61),它们被 TLR3 和 TLR4 配体显著上调。相比之下,TRIM59 的表达在 TLR3 和 TLR4 配体激活的人和小鼠巨噬细胞中均下调。Western blot 验证了 TRIM 蛋白的变化。最后,TRIM59 的过表达显著抑制 LPS 诱导的巨噬细胞活化,而 siRNA 介导的 TRIM59 敲低增强了 LPS 诱导的巨噬细胞活化。总之,该研究深入了解了 TLR 配体诱导的巨噬细胞中 TRIM 家族的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f47/5314404/c0bef2e0f0a6/srep42781-f1.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验