• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

炎症性肠病中 TRAF3 和 TRAF5 的上调和预先激活。

Up-regulation and pre-activation of TRAF3 and TRAF5 in inflammatory bowel disease.

机构信息

Division of Gastroenterology and Hepatology, Shanghai Jiao-Tong University School of Medicine Renji Hospital, Shanghai Institute of Digestive Disease; Key Laboratory of Gastroenterology & Hepatology, Ministry of Health (Shanghai Jiao-Tong University). 145 Middle Shandong Rd, Shanghai 200001, China.

出版信息

Int J Med Sci. 2013;10(2):156-63. doi: 10.7150/ijms.5457. Epub 2013 Jan 3.

DOI:10.7150/ijms.5457
PMID:23329887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3547213/
Abstract

OBJECTIVE

TRAF3 and TRAF5 share a common ancestral gene, and interact as essential components of signaling pathways in immunity. TRAF3 and TRAF5 are overexpressed in the colon of rat/mouse models with colitis. However, the expressions of TRAF3 and TRAF5 in patients with inflammatory bowel disease have not been elucidated. The aim of the present study is to explore the potential roles of TRAF3 and TRAF5 in patients with inflammatory bowel disease.

METHODS

Plasma levels of TRAF3 and TRAF5 proteins were detected by Enzyme-linked Immunosorbent Assay (ELISA). Colonic expression of TRAF3 and TRAF5 proteins was detected by western blot analysis. Quantitative Real-time PCR (qRT-PCR) was applied for gene expression. Inflamed intestinal mucosa and non-inflamed intestinal mucosa in patients with inflammatory bowel disease and normal mucosa was analyzed from healthy controls.

RESULTS

The plasma levels of TRAF3 and TRAF5 were significantly higher both in patients with Crohn's disease and ulcerative colitis than in healthy controls. Only soluble TRAF5 showed a weak correlation with endoscopic disease activity index (Baron score) in patients with ulcerative colitis (spearman's r=0.358, P=0.022). Gene expressions of TRAF3 and TRAF5 in peripheral blood mononuclear cells were significantly higher both in patients with Crohn's disease and ulcerative colitis than in healthy controls (all P<0.0001). Gene and protein expressions of TRAF3 and TRAF5 were significantly higher in inflamed colonic mucosa of patients with Crohn's disease and ulcerative colitis than in non-inflamed colonic mucosa and normal mucosa of healthy controls (all P<0.0001). Furthermore, gene and protein expressions of TRAF3 and TRAF5 were also significantly higher in non-inflamed colonic mucosa of patients with Crohn's disease and ulcerative colitis than in normal mucosa of healthy controls.

CONCLUSIONS

TRAF3 and TRAF5 are overexpressed in inflammatory bowel disease. Although the endoscopic appearance can be normal, TRAF3 and TRAF5 pre-activation can be detected in non-inflamed colonic segments.

摘要

目的

TRAF3 和 TRAF5 拥有共同的祖先基因,并作为免疫信号通路的必需组成部分相互作用。TRAF3 和 TRAF5 在结肠炎大鼠/小鼠模型的结肠中过度表达。然而,TRAF3 和 TRAF5 在炎症性肠病患者中的表达尚未阐明。本研究旨在探讨 TRAF3 和 TRAF5 在炎症性肠病患者中的潜在作用。

方法

通过酶联免疫吸附测定(ELISA)检测 TRAF3 和 TRAF5 蛋白的血浆水平。通过 Western blot 分析检测 TRAF3 和 TRAF5 蛋白的结肠表达。应用定量实时 PCR(qRT-PCR)进行基因表达分析。从健康对照者中分析炎症性肠病患者的炎症性和非炎症性肠黏膜与正常黏膜。

结果

克罗恩病和溃疡性结肠炎患者的 TRAF3 和 TRAF5 血浆水平均明显高于健康对照组。仅可溶性 TRAF5 与溃疡性结肠炎患者的内镜疾病活动指数(Baron 评分)呈弱相关(spearman's r=0.358,P=0.022)。克罗恩病和溃疡性结肠炎患者外周血单个核细胞中 TRAF3 和 TRAF5 的基因表达均明显高于健康对照组(均 P<0.0001)。克罗恩病和溃疡性结肠炎患者的炎症性结肠黏膜中 TRAF3 和 TRAF5 的基因和蛋白表达均明显高于非炎症性结肠黏膜和健康对照组的正常黏膜(均 P<0.0001)。此外,克罗恩病和溃疡性结肠炎患者的非炎症性结肠黏膜中 TRAF3 和 TRAF5 的基因和蛋白表达也明显高于健康对照组的正常黏膜。

结论

TRAF3 和 TRAF5 在炎症性肠病中过度表达。尽管内镜表现可能正常,但在非炎症性结肠节段也可检测到 TRAF3 和 TRAF5 的预激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f66b/3547213/917ad724cf09/ijmsv10p0156g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f66b/3547213/c4d0f18fda1f/ijmsv10p0156g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f66b/3547213/ad4a20f4db8f/ijmsv10p0156g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f66b/3547213/917ad724cf09/ijmsv10p0156g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f66b/3547213/c4d0f18fda1f/ijmsv10p0156g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f66b/3547213/ad4a20f4db8f/ijmsv10p0156g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f66b/3547213/917ad724cf09/ijmsv10p0156g03.jpg

相似文献

1
Up-regulation and pre-activation of TRAF3 and TRAF5 in inflammatory bowel disease.炎症性肠病中 TRAF3 和 TRAF5 的上调和预先激活。
Int J Med Sci. 2013;10(2):156-63. doi: 10.7150/ijms.5457. Epub 2013 Jan 3.
2
Analysis of direct tissue isoelectric focused protein profiles of resected intestinal mucosa and endoscopic biopsies from patients with inflammatory bowel disease.炎症性肠病患者切除的肠黏膜和内镜活检组织的直接组织等电聚焦蛋白质谱分析。
Clin Invest Med. 1992 Feb;15(1):49-59.
3
Immunohistochemical localization of vascular endothelial growth factor in colonic mucosa of patients with inflammatory bowel disease.血管内皮生长因子在炎症性肠病患者结肠黏膜中的免疫组织化学定位
Hepatogastroenterology. 2002 Jan-Feb;49(43):116-23.
4
Increased production of vascular endothelial growth factor by intestinal mucosa of patients with inflammatory bowel disease.炎症性肠病患者肠黏膜中血管内皮生长因子的产生增加。
Hepatogastroenterology. 1999 Mar-Apr;46(26):920-3.
5
Development, validation and implementation of an in vitro model for the study of metabolic and immune function in normal and inflamed human colonic epithelium.用于研究正常和炎症状态下人结肠上皮细胞代谢与免疫功能的体外模型的开发、验证及应用
Dan Med J. 2015 Jan;62(1):B4973.
6
CD40 and CD86 upregulation with divergent CMRF44 expression on blood dendritic cells in inflammatory bowel diseases.炎症性肠病中血液树突状细胞上CD40和CD86上调且CMRF44表达存在差异
Am J Gastroenterol. 2001 Oct;96(10):2946-56. doi: 10.1111/j.1572-0241.2001.04686.x.
7
Opposite effects of interferon regulatory factor 1 and osteopontin on the apoptosis of epithelial cells induced by TNF-α in inflammatory bowel disease.干扰素调节因子1和骨桥蛋白对炎症性肠病中TNF-α诱导的上皮细胞凋亡的相反作用。
Inflamm Bowel Dis. 2014 Nov;20(11):1950-61. doi: 10.1097/MIB.0000000000000192.
8
Increased nitric oxide production and inducible nitric oxide synthase activity in colonic mucosa of patients with active ulcerative colitis and Crohn's disease.活动期溃疡性结肠炎和克罗恩病患者结肠黏膜中一氧化氮生成增加及诱导型一氧化氮合酶活性增强。
Dig Dis Sci. 1997 May;42(5):1047-54. doi: 10.1023/a:1018849405922.
9
Increased interleukin 8 expression in the colon mucosa of patients with inflammatory bowel disease.炎症性肠病患者结肠黏膜中白细胞介素8表达增加。
Gut. 1996 Feb;38(2):216-22. doi: 10.1136/gut.38.2.216.
10
Increased group II phospholipase A2 in colonic mucosa of patients with Crohn's disease and ulcerative colitis.克罗恩病和溃疡性结肠炎患者结肠黏膜中Ⅱ型磷脂酶A2增加。
Gut. 1994 Nov;35(11):1593-8. doi: 10.1136/gut.35.11.1593.

引用本文的文献

1
A New Differential Gene Expression Based Simulated Annealing for Solving Gene Selection Problem: A Case Study on Eosinophilic Esophagitis and Few Other Gastro-intestinal Diseases.一种基于差异基因表达的新型模拟退火算法用于解决基因选择问题:嗜酸性食管炎及其他几种胃肠道疾病的案例研究
Biochem Genet. 2024 Dec 6. doi: 10.1007/s10528-024-10987-z.
2
Circular RNA SMARCA5 inhibits cholangiocarcinoma via microRNA-95-3p/tumor necrosis factor receptor associated factor 3 axis.环状 RNA SMARCA5 通过 microRNA-95-3p/肿瘤坏死因子受体相关因子 3 轴抑制胆管癌。
Anticancer Drugs. 2023 Oct 1;34(9):1002-1009. doi: 10.1097/CAD.0000000000001487. Epub 2023 Jan 24.
3

本文引用的文献

1
Predictors of aggressive inflammatory bowel disease.侵袭性炎症性肠病的预测因素。
Gastroenterol Hepatol (N Y). 2011 Oct;7(10):652-9.
2
Identification of functionally distinct TRAF proinflammatory and phosphatidylinositol 3-kinase/mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (PI3K/MEK) transforming activities emanating from RET/PTC fusion oncoprotein.鉴定源于 RET/PTC 融合癌蛋白的具有不同功能的 TRAF 促炎和磷酸肌醇 3-激酶/丝裂原激活蛋白激酶/细胞外信号调节激酶激酶(PI3K/MEK)转化活性。
J Biol Chem. 2012 Feb 3;287(6):3691-703. doi: 10.1074/jbc.M111.322677. Epub 2011 Dec 9.
3
Roles of tumor necrosis factor receptor associated factor 3 (TRAF3) and TRAF5 in immune cell functions.
Supplementation with Milk-Derived Extracellular Vesicles Shapes the Gut Microbiota and Regulates the Transcriptomic Landscape in Experimental Colitis.
补充乳源细胞外囊泡可塑造肠道微生物群并调节实验性结肠炎的转录组图谱。
Nutrients. 2022 Apr 26;14(9):1808. doi: 10.3390/nu14091808.
4
The Role of E3 Ubiquitin Ligases and Deubiquitinases in Inflammatory Bowel Disease: Friend or Foe?E3 泛素连接酶和去泛素化酶在炎症性肠病中的作用:是敌是友?
Front Immunol. 2021 Dec 8;12:769167. doi: 10.3389/fimmu.2021.769167. eCollection 2021.
5
Structural feature of TRAFs, their related human diseases and therapeutic intervention.肿瘤坏死因子受体相关因子(TRAFs)的结构特征、相关人类疾病及治疗干预
Arch Pharm Res. 2021 May;44(5):475-486. doi: 10.1007/s12272-021-01330-w. Epub 2021 May 10.
6
Role of RING-Type E3 Ubiquitin Ligases in Inflammatory Signalling and Inflammatory Bowel Disease.RING 型 E3 泛素连接酶在炎症信号转导和炎症性肠病中的作用。
Mediators Inflamm. 2020 Aug 10;2020:5310180. doi: 10.1155/2020/5310180. eCollection 2020.
7
Tumor Necrosis Factor Receptor-Associated Factor Regulation of Nuclear Factor κB and Mitogen-Activated Protein Kinase Pathways.肿瘤坏死因子受体相关因子对核因子 κB 和丝裂原活化蛋白激酶通路的调节作用。
Front Immunol. 2018 Aug 9;9:1849. doi: 10.3389/fimmu.2018.01849. eCollection 2018.
8
An integrative network-based approach to identify novel disease genes and pathways: a case study in the context of inflammatory bowel disease.一种基于整合网络的方法来识别新的疾病基因和通路:以炎症性肠病为例的研究。
BMC Bioinformatics. 2018 Jul 13;19(1):264. doi: 10.1186/s12859-018-2251-x.
9
TRAF molecules in inflammation and inflammatory diseases.炎症和炎性疾病中的肿瘤坏死因子受体相关因子分子
Curr Pharmacol Rep. 2018 Feb;4(1):64-90. doi: 10.1007/s40495-017-0117-y. Epub 2017 Dec 20.
10
Emerging Roles for Noncanonical NF-κB Signaling in the Modulation of Inflammatory Bowel Disease Pathobiology.非经典NF-κB信号通路在炎症性肠病病理生物学调节中的新作用
Inflamm Bowel Dis. 2016 Sep;22(9):2265-79. doi: 10.1097/MIB.0000000000000858.
肿瘤坏死因子受体相关因子 3(TRAF3)和 TRAF5 在免疫细胞功能中的作用。
Immunol Rev. 2011 Nov;244(1):55-74. doi: 10.1111/j.1600-065X.2011.01055.x.
4
Expanding TRAF function: TRAF3 as a tri-faced immune regulator.拓展 TRAF 功能:TRAF3 作为一个三面向的免疫调控因子。
Nat Rev Immunol. 2011 Jun 10;11(7):457-68. doi: 10.1038/nri2998.
5
Pattern recognition scavenger receptor CD204 attenuates Toll-like receptor 4-induced NF-kappaB activation by directly inhibiting ubiquitination of tumor necrosis factor (TNF) receptor-associated factor 6.模式识别清道夫受体 CD204 通过直接抑制肿瘤坏死因子(TNF)受体相关因子 6 的泛素化来减弱 Toll 样受体 4 诱导的 NF-κB 激活。
J Biol Chem. 2011 May 27;286(21):18795-806. doi: 10.1074/jbc.M111.224345. Epub 2011 Apr 1.
6
Molecular mechanisms of TNFR-associated factor 6 (TRAF6) utilization by the oncogenic viral mimic of CD40, latent membrane protein 1 (LMP1).肿瘤病毒模拟物 CD40 的潜伏膜蛋白 1(LMP1)利用肿瘤坏死因子受体相关因子 6(TRAF6)的分子机制。
J Biol Chem. 2011 Mar 25;286(12):9948-55. doi: 10.1074/jbc.M110.185983. Epub 2011 Jan 24.
7
TNF receptor-associated factor 3 is required for T cell-mediated immunity and TCR/CD28 signaling.肿瘤坏死因子受体相关因子 3 对于 T 细胞介导的免疫和 TCR/CD28 信号转导是必需的。
J Immunol. 2011 Jan 1;186(1):143-55. doi: 10.4049/jimmunol.1000290. Epub 2010 Nov 17.
8
Human TRAF3 adaptor molecule deficiency leads to impaired Toll-like receptor 3 response and susceptibility to herpes simplex encephalitis.人类 TRAF3 衔接子分子缺陷导致 Toll 样受体 3 反应受损和易患单纯疱疹脑炎。
Immunity. 2010 Sep 24;33(3):400-11. doi: 10.1016/j.immuni.2010.08.014. Epub 2010 Sep 9.
9
Differential B-lymphocyte regulation by CD40 and its viral mimic, latent membrane protein 1.CD40 及其病毒模拟物潜伏膜蛋白 1 对 B 淋巴细胞的差异调节。
Immunol Rev. 2010 Sep;237(1):226-48. doi: 10.1111/j.1600-065X.2010.00932.x.
10
TRAF5 deficiency accelerates atherogenesis in mice by increasing inflammatory cell recruitment and foam cell formation.TRAF5 缺乏通过增加炎症细胞募集和泡沫细胞形成加速小鼠动脉粥样硬化形成。
Circ Res. 2010 Sep 17;107(6):757-66. doi: 10.1161/CIRCRESAHA.110.219295. Epub 2010 Jul 22.