...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Translational research: the journal of laboratory and clinical medicine >Role of regenerating gene I in claudin expression and barrier function in the small intestine
【24h】

Role of regenerating gene I in claudin expression and barrier function in the small intestine

机译：再生基因I在小肠claudin表达和屏障功能中的作用

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We have recently shown that loss of the regenerating gene (Reg) I causes susceptibility to nonsteroidal anti-inflammatory drug-induced gastrointestinal damage. However, the mechanism by which Reg I plays a protective role against this pathophysiological condition is unclear. Here, we investigated whether Reg I plays roles in the induction of tight junction proteins and mucosal barrier function in the small intestine. The small-intestinal permeability was evaluated in Reg I-deficient mice by FITC-dextran and transepithelial electrical resistance (TEER) assay. The effect of REG I alpha on TEER, claudins expression, and intracellular signaling was examined using Caco2 cells in vitro. Small-intestinal expression of claudins 3 and 4 was investigated in Reg I-deficient mice in vivo. REG I deficiency significantly decreased the expression of claudin 3 in the small-intestinal epithelium. When mice were treated with indomethacin, the serum level of FITC-dextran in Reg 1 knockout mice was significantly higher than that in wild-type (WT) mice. The level of small-intestinal TEER was significantly decreased in Reg I alpha knockout mice compared with WT mice under normal condition. REG I alpha stimulation significantly enhanced the level of TEER in Caco2 cells. Treatment with REG la enhanced the expression of claudins 3 and 4 and promoted Sp1, Akt, and ERK phosphorylation in Caco2 cells, whereas these effects were attenuated by treatment with anti-REG I alpha antibody. Reg I may play a role in the maintenance of mucosal barrier function by inducing tight junction proteins such as claudins 3 and 4.
机译：我们最近发现，再生基因（Reg）I的缺失会导致非甾体类抗炎药诱发的胃肠道损伤。但是，Reg I对这种病理生理状况起保护作用的机制尚不清楚。在这里，我们调查了Reg I是否在小肠中紧密连接蛋白的诱导和粘膜屏障功能的诱导中发挥作用。通过FITC-葡聚糖和经上皮电阻（TEER）分析评估Reg I缺陷小鼠的小肠通透性。在体外使用Caco2细胞检查了REG Iα对TEER，claudins表达和细胞内信号传导的影响。在体内Reg I缺陷的小鼠中研究了claudins 3和4的小肠表达。 REG I缺乏显着降低小肠上皮中claudin 3的表达。当用吲哚美辛治疗小鼠时，Reg 1基因敲除小鼠的FITC-右旋糖酐血清水平明显高于野生型（WT）小鼠。与正常条件下的WT小鼠相比，Reg Iα基因敲除小鼠的小肠TEER水平显着降低。 REG Iα刺激显着增强了Caco2细胞中TEER的水平。 REG 1a处理增强了Caco2细胞中claudins 3和4的表达，并促进了Sp1，Akt和ERK磷酸化，而抗REG Iα抗体处理则减弱了这些作用。 Reg I可能通过诱导紧密连接蛋白（例如claudins 3和4）来维持黏膜屏障功能。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号