权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Biological modulation of the epithelial-mesenchymal interaction in gut wound repair process.

肠道伤口修复过程中上皮间质相互作用的生物调节。

基本信息

批准号：
10670503
负责人：
WATANABE Sumio
金额：
$ 1.98万
依托单位：
AKITA UNIVERSITY (1999)Juntendo University (1998)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

项目摘要

It has been generally accepted that the epithelial-mesenchymal interaction plays an important role in gut would repair process. In this project, we investigated the detailed mechanism of action of several growth factors, cytokines, ECM, toxic agents, trace minerals and physical stress in gut would healing using in vivo and in vitro would healing model. As expected, each growth factor has its own target cells and some growth factors show their effects by paracrine and autocrine mechanism. Among these growth factors, insulin-like growth factor 1 played a key role in gastric wound healing in vivo and in vitro. In this mechanism zinc stimulated the production of insulin-like growth factor 1 from fibroblasts and endothelial cells and induced insulin-like growth factor 1 affected to gastric epithelial cell migration and proliferation. In another series of experiments, we showed that heat shock protein 72 has cytoprotective effect in the stomach and pre-induction of heat shock protein 72 prevented gastric mucosal damage in the several experimental model with rats. In the experiment using strain stress in vitro, heat shock protein 72 was found in decreased significantly in the gastric epithelial cells and strain stress also inhibited gastric epithelial migration and proliferation resulting in the delay of wound healing. In the clinical situation, we found the inhibition of the heat shock protein expression in the Helicobacter pylori infected gastric mucosa. Therefore heat shock protein as well as growth factors may play an important role in the integrity of gastric mucosal damage and wound healing.

人们普遍认为上皮间质相互作用在肠道修复过程中起着重要作用。在这个项目中，我们使用体内和体外伤口愈合模型研究了几种生长因子、细胞因子、ECM、有毒物质、微量矿物质和物理压力在肠道愈合中的详细作用机制。正如预期的那样，每种生长因子都有其自己的靶细胞，并且一些生长因子通过旁分泌和自分泌机制发挥作用。在这些生长因子中，胰岛素样生长因子1在体内和体外胃伤口愈合中发挥着关键作用。在这一机制中，锌刺激成纤维细胞和内皮细胞产生胰岛素样生长因子1，并诱导胰岛素样生长因子1影响胃上皮细胞迁移和增殖。在另一系列实验中，我们发现热休克蛋白72对胃具有细胞保护作用，并且热休克蛋白72的预诱导在多个大鼠实验模型中可以预防胃粘膜损伤。在体外应变应力实验中发现，胃上皮细胞中热休克蛋白72显着减少，应变应力还抑制胃上皮迁移和增殖，导致伤口愈合延迟。在临床情况中，我们发现幽门螺杆菌感染的胃粘膜中热休克蛋白的表达受到抑制。因此，热休克蛋白以及生长因子可能在胃粘膜损伤的完整性和伤口愈合中发挥重要作用。