• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Expression of transforming growth factor beta (TGF-beta 1) in human epithelial alveolar cells: a pro-inflammatory mediator independent pathway
【24h】

Expression of transforming growth factor beta (TGF-beta 1) in human epithelial alveolar cells: a pro-inflammatory mediator independent pathway

机译：转化生长因子β（TGF-β1）在人上皮肺泡细胞中的表达：促炎介质独立途径

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

Regulation of transforming growth factor beta 1 (TGF-beta1) expression remains unclear. Inflammation has been inferred to play a major role in stimulating TGF-beta1 production since high concentrations of TGF-beta1 have been found in the lungs of patients with various diffuse inflammatory lung diseases. To establish an association between inflammation and TGF-beta1 expression, human alveolar epithelial (A549) cells were co-cultured with lipopolysaccharide (LPS), Tumor necrosis factor alpha (TNFalpha), Interleukin 1 beta (IL-1beta) and Interleukin 8 (IL-8) for 12 hours. Total and bioactive TGF-beta1 protein were then measured. A549 cells transiently transfected with a plasmid containing the TGF-beta1 promoter linked to a luciferase reported gene were then co-cultured with the same inflammatory peptides for 12 hours and TGF-beta1 promoter activity determined. Nuclear transcription factors AP-1 (c-jun) or NF-kappa (p65, p50 and p105) were over expressed in A549 cells transiently transfected with the TGF-beta1 promoter and TGF-beta1 promoter activity subsequently measured. Stimulation with inflammatory signals LPS, TNFalpha, IL-1beta, IL-8 resulted in no increase of total or bioactive TGF-beta1 activity above constitutive concentrations in vitro. TGF-beta1 promoter activity was also unchanged from baseline levels in response to the same inflammatory peptides. Expression of c-jun however led to significant increases of TGF-beta1 promoter activity over constitutive levels. In contrast p65 and p105 expression resulted in inhibition of TGF-beta1 promoter activity below baseline levels. We conclude that in a human alveolar epithelial cell line, inflammation does not regulate TGF-beta1 expression. These studies suggest that in lung pathologies such as asthma,jung fibrosis and CLD, TGF-beta1 production may involve pathways independent of inflammatory mediators LPS, TNFalpha, IL-1beta and IL-8. (C) 2004 Elsevier Inc. All rights reserved.
机译：转化生长因子β1（TGF-beta1）表达的调节尚不清楚。由于在患有各种弥漫性炎症性肺病的患者的肺部发现了高​​浓度的TGF-β1，因此炎症被认为在刺激TGF-β1产生中起主要作用。为了建立炎症与TGF-β1表达之间的联系，将人肺泡上皮（A549）细胞与脂多糖（LPS），肿瘤坏死因子α（TNFalpha），白介素1 beta（IL-1beta）和白介素8（IL）共培养-8）持续12小时。然后测量了总的和具有生物活性的TGF-beta1蛋白。然后将用含有连接至萤光素酶报道基因的TGF-β1启动子的质粒瞬时转染的A549细胞与相同的炎症肽共培养12小时，并确定TGF-β1启动子的活性。核转录因子AP-1（c-jun）或NF-κ（p65，p50和p105）在用TGF-beta1启动子瞬时转染的A549细胞中过表达，随后测量了TGF-beta1启动子的活性。用炎症信号LPS，TNFalpha，IL-1beta，IL-8刺激不会导致总的或具有生物活性的TGF-beta1活性高于体外组成浓度。响应相同的炎症肽，TGF-beta1启动子活性也未从基线水平改变。然而，c-jun的表达导致TGF-beta1启动子活性明显高于组成型水平。相反，p65和p105表达导致TGF-beta1启动子活性低于基线水平。我们得出的结论是，在人的肺泡上皮细胞系中，炎症不会调节TGF-beta1的表达。这些研究表明，在诸如哮喘，中肠纤维化和CLD之类的肺部疾病中，TGF-β1的产生可能涉及独立于炎症介质LPS，TNFα，IL-1β和IL-8的途径。 （C）2004 Elsevier Inc.保留所有权利。

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