• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >E-cadherin promotes EGFR-mediated cell differentiation and MUC5AC mucin expression in cultured human airway epithelial cells.
【24h】

E-cadherin promotes EGFR-mediated cell differentiation and MUC5AC mucin expression in cultured human airway epithelial cells.

机译：E-钙粘着蛋白在培养的人气道上皮细胞中促进EGFR介导的细胞分化和MUC5AC粘蛋白表达。

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

In previous work, we showed that epidermal growth factor receptor (EGFR) activation causes mucin expression in airway epithelium in vivo and in human NCI-H292 airway epithelial cells and normal human bronchial epithelial (NHBE) cells in vitro. Here we show that the cell surface adhesion molecule, E-cadherin, promotes EGFR-mediated mucin production in NCI-H292 cells in a cell density- and cell cycle-dependent fashion. The addition of the EGFR ligand, transforming growth factor (TGF)-alpha, increased MUC5AC protein expression markedly in dense, but not in sparse, cultures. MUC5AC-positive cells in dense cultures contained 2 N DNA content and did not incorporate bromodeoxyuridine, suggesting that they develop via cell differentiation and that a surface molecule involved in cell-cell contact is important for EGFR-mediated mucin production. In support of this hypothesis, in dense cultures of NCI-H292 cells and in NHBE cells at air-liquid interface, blockade of E-cadherin-mediated cell-cell contacts decreased EGFR-dependent mucin production. E-cadherin blockade also increased EGFR-dependent cell proliferation and TGF-alpha-induced EGFR tyrosine phosphorylation in dense cultures of NCI-H292 cells, suggesting that E-cadherin promotes EGFR-dependent mucin production and inhibits EGFR-dependent cell proliferation via modulation of EGFR phosphotyrosine levels. Furthermore, in dense cultures, E-cadherin blockade decreased the rate of EGFR tyrosine dephosphorylation, implicating an E-cadherin-dependent protein tyrosine phosphatase in EGFR dephosphorylation. Thus E-cadherin promotes EGFR-mediated cell differentiation and MUC5AC production, and our results suggest that this occurs via a pathway involving protein tyrosine phosphatase-dependent EGFR dephosphorylation.
机译：在先前的工作中，我们表明表皮生长因子受体（EGFR）的激活会导致黏蛋白在体内气道上皮以及体外人NCI-H292气道上皮细胞和正常人支气管上皮（NHBE）细胞中表达。在这里，我们显示细胞表面粘附分子E-钙粘着蛋白以细胞密度和细胞周期依赖性方式促进NCI-H292细胞中EGFR介导的粘蛋白生成。 EGFR配体（转化生长因子（TGF）-α）的添加在致密（而不是稀疏）培养物中显着提高了MUC5AC蛋白表达。密集培养物中的MUC5AC阳性细胞含有2 N DNA含量，并且没有掺入溴脱氧尿苷，这表明它们是通过细胞分化而发育的，参与细胞与细胞接触的表面分子对于EGFR介导的粘蛋白生产很重要。支持该假设的是，在NCI-H292细胞的密集培养物中和气液界面的NHBE细胞中，E-钙粘蛋白介导的细胞间接触的阻断降低了EGFR依赖性粘蛋白的产生。在NCI-H292细胞的密集培养物中，E-钙粘蛋白的阻滞也增加了EGFR依赖的细胞增殖和TGF-α诱导的EGFR酪氨酸磷酸化，这表明E-钙粘着蛋白可通过调节EGFR来促进EGFR依赖的粘蛋白生成并抑制EGFR依赖的细胞增殖。 EGFR磷酸酪氨酸水平。此外，在致密培养中，E-钙粘蛋白的阻断降低了EGFR酪氨酸脱磷酸的速率，这意味着E-钙粘蛋白依赖性蛋白酪氨酸磷酸酶参与了EGFR的去磷酸化。因此，E-钙粘着蛋白促进EGFR介导的细胞分化和MUC5AC的产生，我们的结果表明这是通过涉及蛋白酪氨酸磷酸酶依赖性EGFR脱磷酸作用的途径发生的。

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