Role of tumor-suppressive genes on LPS-induced inflammatory response

肿瘤抑制基因在 LPS 诱导的炎症反应中的作用

• 批准号: 22590408
• 负责人: YOKOCHI Takashi
• 金额: $ 2.91万
• 依托单位: Aichi Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22590408/
• 关键词: LPS; ASAP1; RAW264.7 NF-kappaB; 炎症性メディエーター; RIZ1; NF-kappaB; 一酸化窒素; がん遺伝子; サイトカイン; MAPK; 癌遺伝子; retinoblastoma protein-interacting zinc finger1; p53; RAW264.7; TNF-alpha

The involvement of retinoblastoma protein-interacting zinc finger 1 (RIZ1), a tumor suppressor, in lipopolysaccharide (LPS)-induced inflammatory responses was investigated by using RAW 264.7 macrophage-like cells. RIZ1 was suggested to augment LPS-induced NF-kappaB activation in collaboration with p53 and enhance the production of proinflammatory cytokines in response to LPS. An ADP ribosylation factor-GTPase activating protein (ASAP1) is constitutively expressed in the cells and the expression was augmented by LPS stimulation. Silencing of ASAP1 enhanced the production of proinflammatory mediators in response to LPS. A series of tumor-associated genes are involved in LPS-induced inflammatory response in macrophages.

利用RAW 264.7巨噬细胞样细胞研究了肿瘤抑制因子视网膜母细胞瘤蛋白相互作用锌指1（RIZ 1）在脂多糖（LPS）诱导的炎症反应中的作用。RIZ 1被认为与p53协同增强LPS诱导的NF-κ B活化，并增强响应于LPS的促炎细胞因子的产生。ADP核糖基化因子-GTP酶激活蛋白（ASAP 1）在细胞中组成性表达，LPS刺激可增强其表达。ASAP 1的沉默增强了响应LPS的促炎介质的产生。一系列肿瘤相关基因参与LPS诱导的巨噬细胞炎症反应。

项目成果

A new experimental murine model for lipopolysaccharide-mediated lethal shock with lung injury

• DOI: 10.1177/1753425911410236
• 发表时间: 2012-04
• 期刊: Innate Immunity
• 影响因子: 3.2
• 作者: T. Yokochi

An ADP ribosylation factor-GTPase activating protein negatively regulates the production of proinflammatory mediators in response to lipopolysaccharide

• DOI: 10.1007/s00262-011-1048-9
• 发表时间: 2011-10-01
• 期刊: CANCER IMMUNOLOGY IMMUNOTHERAPY
• 影响因子: 5.8
• 作者: Haque, Abedul;Noman, Abu Shadat Mohammod;Yokochi, Takashi
• 通讯作者: Yokochi, Takashi

ONO 3403, a synthetic serine protease inhibitor, inhibits lipopolysacchar ide-induced tumor necrosis factor-{alpha} and nitric oxide production and protects mice from lethal endotoxic shock

ONO 3403 是一种合成丝氨酸蛋白酶抑制剂，可抑制脂多糖诱导的肿瘤坏死因子-{α} 和一氧化氮的产生，并保护小鼠免受致命的内毒素休克

• 发表时间: 2011
• 期刊: Innate Immun
• 作者: Tumurkhuu G.;et al.
• 通讯作者: et al.

on lipopolysaccharide-induced nitric oxide via reducing interferon-ss production.The novel inhibitory effect of pifithrin (PFT)-α, an inhibitor of p53

通过减少干扰素-SS 的产生，对脂多糖诱导的一氧化氮产生影响。 p53 抑制剂 Pifithrin (PFT)-α 的新型抑制作用

• 发表时间: 2012
• 作者: Badamtseren B;et al.;Erdenezaya Odkhuu et al.
• 通讯作者: Erdenezaya Odkhuu et al.

Low susceptibility of NC/Nga mice to the lipopolysaccharide-mediated lethality with D-galactosamine sensitization and the involvement of fewer natural killer T cells

NC/Nga 小鼠对 D-半乳糖胺致敏和较少自然杀伤 T 细胞参与的脂多糖介导的致死作用的敏感性较低

• DOI: 10.1177/1753425910390400
• 发表时间: 2012
• 期刊: Innate Immun
• 作者: 大野尚仁;安達禎之;三浦典子;石橋健一;飛田敏江;山中大輔;Tanigawa T;Mendjargal A;Koide N
• 通讯作者: Koide N