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A study of inflammatory bowel diseases using Smad2 conditional knockout mice.

使用 Smad2 条件敲除小鼠进行炎症性肠病研究。

基本信息

批准号：
16590603
负责人：
NAKAMURA Kazuhiko
金额：
$ 1.98万
依托单位：
KYUSHU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2005
项目状态：
已结题

项目摘要

<Generation and analysis of T cell-specific Smad2 conditional knockout mice>Lck-Cre transgenic mice, which express Cre recombinase in a T cell-specific manner, was mated with Smad2^<+/-> mice and Lck-Cre Smad2^<+/-> mice were obtained. Then, Lck-Cre Smad2^<+/-> mice were mated with Smad2^<flox/flox> mice and Smad2^<flox/+>, Smad2^<flox/->, Lck-Cre Smad2^<flox/+> and Lck-Cre Smad2^<flox/-> mice were generated. Smad2 expression was down-regulated, but was not absent, in T cells from Lck-Cre Smad2^<flox/->. Spontaneous colitis was not observed in Lck-Cre Smad2^<flox/-> mice. In the dextran sulphate sodium induce colitis model and the oxazolone enema colitis model, there was not a significant difference in the level of colitis and expression of cytokines in colon between Smad2^<flox/+> and Lck-Cre Smad2^<flox/->.<Generation of macrophage/neutrophil-specific Smad2 conditional knockout mice>Smad2^<+/-> mice were mated with LysMcre mice, which express Cre recombinase in a macrophage/neutrophil-specific fashion, and LysMcre-Smad2^<flox/+> was obtained. Then, LysMcre-Smad2^<flox/+> was mated with Smad2^<flox/flox> mice and Smad2^<flox/+>, Smad2^<flox/flox>, LysMcre-Smad2^<flox/+> and LysMcre-Smad2^<flox/flox> mice were generated. In macrophages from LysMcre-Smad2^<flox/flox> mice, the expression of Smad2 was significantly decreased but was not absent. Spontaneous colitis was not observed in LysMcre-Smad2^<flox/flox> mice.<Conclusion>The evidence for the importance of Smad2 signaling in T cells or in macrophages and neutrophils for regulation of intestinal inflammation was not obtained.

<Generation and analysis of T cell-specific Smad2 conditional knockout mice>将以T细胞特异性方式表达Cre重组酶的Lck-Cre转基因小鼠与Smad 2 ^<+/->小鼠交配，获得Lck-Cre Smad 2 ^<+/->小鼠。然后，将Lck-Cre Smad 2 ^<+/->小鼠与Smad 2 ^<flox/flox>小鼠交配，并产生Smad 2 ^<flox/+>、Smad 2 ^<flox/->、Lck-Cre Smad 2 ^<flox/+>和Lck-Cre Smad 2 ^<flox/->小鼠。Smad 2表达下调，但不是不存在，在T细胞从Lck-Cre Smad 2 ^<flox/->。在Lck-Cre Smad 2 +<flox/->小鼠中未观察到自发性结肠炎。在葡聚糖硫酸钠诱导的结肠炎模型和恶唑酮灌肠结肠炎模型中，Smad 2 ^<flox/+>和Lck-Cre Smad 2 ^<flox/->之间的结肠炎水平和结肠中细胞因子的表达没有显著差异。<巨噬细胞/嗜中性粒细胞特异性Smad 2条件性敲除小鼠的产生>将Smad 2 ^<+/->小鼠与以巨噬细胞/嗜中性粒细胞特异性方式表达Cre重组酶的LysMcre小鼠交配，并获得LysMcre-Smad 2 ^<flox/+>。然后，使LysMcre-Smad 2 ^<flox/+>与Smad 2 ^<flox/flox>小鼠交配，并产生Smad 2 ^<flox/+>、Smad 2 ^<flox/flox>、LysMcre-Smad 2 ^<flox/+>和LysMcre-Smad 2 ^<flox/flox>小鼠。在LysMcre-Smad 2 ^<flox/flox>小鼠的巨噬细胞中，Smad 2的表达显着减少，但并非不存在。在LysMcre-Smad 2 +<flox/flox>小鼠中未观察到自发性结肠炎。<Conclusion>尚未获得Smad 2信号在T细胞或巨噬细胞和中性粒细胞中调节肠道炎症的重要性的证据。

项目成果

期刊论文数量（24）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

A Benzimidazole Fungicide, Benomyl and Its Metabolite Carbendazim Induce Aromatase Activity in Human Ovarian Granulose-Like Tumor Cell Line (KGN).

苯并咪唑类杀菌剂苯菌灵及其代谢物多菌灵可诱导人卵巢颗粒样肿瘤细胞系 (KGN) 的芳香酶活性。

DOI：
发表时间：
2004
期刊：
Endocrinology 145
影响因子：
0
作者：
Morinaga H;Yanase T;Nomura M;Okabe T;Goto K;Harada N et al.
通讯作者：
Harada N et al.

Androgen receptor null male mice develop late-onset obesity caused by decreased energy expenditure and lipolytic activity but show normal insulin sensitivity with high adiponectin secretion

DOI：
10.2337/diabetes.54.4.1000
发表时间：
2005-04-01
期刊：
DIABETES
影响因子：
7.7
作者：
Fan, WQ;Yanase, T;Nawata, H
通讯作者：
Nawata, H

An inverse correlation of human peripheral blood regulatory T cell frequency with the disease activity of ulcerative colitis

DOI：
10.1007/s10620-006-3191-2
发表时间：
2006-04-01
期刊：
DIGESTIVE DISEASES AND SCIENCES
影响因子：
3.1
作者：
Takahashi, M;Nakamura, K;Nawata, H
通讯作者：
Nawata, H

Th1-inducing property of IL-27/WSX-1 signaling is required for the induction of experimental colitis.

IL-27/WSX-1 信号传导的 Th1 诱导特性是诱导实验性结肠炎所必需的。

DOI：
发表时间：
2005
期刊：
Inflammatory Bowel Diseases 11
影响因子：
0
作者：
Hirono H;Ajioka Y;Watanabe H;Baba Y;Tozawa E;Nishikura K;Mukai G;Honma T;Aoyagi Y.;Honda et al.
通讯作者：
Honda et al.

TGF-β1 plays an important role in the mechanism of CD4+CD25+ regulatory T cell activity in both humans and mice