• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Enteric glia inhibit intestinal epithelial cell proliferation partly through a TGF-beta1-dependent pathway.
【24h】

Enteric glia inhibit intestinal epithelial cell proliferation partly through a TGF-beta1-dependent pathway.

机译：肠神经胶质细胞部分通过TGF-beta1依赖性途径抑制肠上皮细胞增殖。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Although recent studies have shown that enteric neurons control intestinal barrier function, the role of enteric glial cells (EGCs) in this control remains unknown. Therefore, our goal was to characterize the role of EGCs in the control of intestinal epithelial cell proliferation using an in vivo transgenic and an in vitro coculture model. Assessment of intestinal epithelial cell proliferation after ablation of EGCs in transgenic mice demonstrated a significant increase in crypt cell hyperplasia. Furthermore, mucosal glial network (assessed by immunohistochemical detection of S-100beta) is altered in colon adenocarcinoma compared with control tissue. In an in vitro coculture model of subconfluent Caco-2 cells seeded onto Transwell filters with EGCs, Caco-2 cell density and [3H]thymidine incorporation were significantly lower than in control (Caco-2 cultured alone). Flow cytometry analysis showed that EGCs had no effect on Caco-2 cell viability. EGCs induced a significant increase in Caco-2 cell surfacearea without any sign of cellular hypertrophy. These effects by EGCs were also seen in various transformed or nontransformed intestinal epithelial cell lines. Furthermore, TGF-beta1 mRNA was expressed, and TGF-beta1 was secreted by EGCs. Exogenously added TGF-beta1 reproduced partly the EGC-mediated effects on cell density and surface area. In addition, EGC effects on Caco-2 cell density were significantly reduced by a neutralizing TGF-beta antibody. In conclusion, EGCs have profound antiproliferative effects on intestinal epithelial cells. Functional alterations in EGCs may therefore modify intestinal barrier functions and be involved in pathologies such as cancer or inflammatory bowel diseases.
机译：尽管最近的研究表明，肠神经元控制肠屏障功能，但肠神经胶质细胞（EGC）在该控制中的作用仍然未知。因此，我们的目标是使用体内转基因和体外共培养模型来表征EGC在控制肠上皮细胞增殖中的作用。消融转基因小鼠中的EGCs后肠道上皮细胞增殖的评估表明隐窝细胞增生明显增加。此外，与对照组织相比，结肠腺癌中的粘膜神经胶质网络（通过S-100beta的免疫组织化学检测评估）发生了改变。在用EGC接种到Transwell滤膜上的亚汇合Caco-2细胞的体外共培养模型中，Caco-2细胞密度和[3H]胸苷掺入均显着低于对照（单独培养Caco-2）。流式细胞仪分析表明，EGC对Caco-2细胞活力没有影响。 EGC诱导Caco-2细胞表面积显着增加，而没有任何细胞肥大迹象。在各种转化的或未转化的肠上皮细胞系中也可见到EGC的这些作用。此外，表达了TGF-β1mRNA，而EGC分泌了TGF-β1。外源添加的TGF-β1部分复制了EGC介导的对细胞密度和表面积的影响。此外，中和的TGF-β抗体显着降低了EGC对Caco-2细胞密度的影响。总之，EGC对肠上皮细胞具有深远的抗增殖作用。因此，EGC中的功能改变可能会改变肠道屏障功能，并参与诸如癌症或炎症性肠病的病理过程。

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