• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Adenovirus vectors activate survival pathways in lung epithelial cells.
【24h】

Adenovirus vectors activate survival pathways in lung epithelial cells.

机译：腺病毒载体激活肺上皮细胞中的存活途径。

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

Airway epithelial cells are often the sites of targeted adenovirus vector delivery. Activation of the host inflammatory response and modulation of signal transduction pathways by adenovirus vectors have been previously documented, including activation of MAP kinases and phosphatidylinositol 3-kinase (PI3-kinase). The effect of activation of these pathways by adenovirus vectors on cell survival has not been examined. Both the PI3-kinase/Akt and ERK/MAP kinase signaling pathways have been linked to cell survival. Akt has been found to play a role in cell survival and apoptosis through its downstream effects on apoptosis-related proteins. Constitutive activation of either PI3-kinase or Akt blocks apoptosis induced by c-Myc, UV radiation, transforming growth factor-beta, Fas, and respiratory syncytial virus infection. We examined the effect of adenovirus vector infection on activation of these prosurvival pathways and its downstream consequences. Airway epithelial cells were transduced with replication-deficient adenoviral vectors containing a nonspecific transgene, green fluorescent protein driven by the cytomegalovirus promoter, or an empty vector with no transgene. They were then exposed to the proapoptotic stimulus actinomycin D plus TNF-alpha, and evidence of apoptosis was evaluated. Compared with the cells treated with actinomycin/TNF alone, the adenovirus vector-infected cells had a 50% reduction in apoptosis. When we examined induction of the prosurvival pathways, ERK and AKT, in the viral vector-infected cells, we found that there was significant activation of both Akt and ERK.
机译：气道上皮细胞通常是靶向腺病毒载体递送的位点。腺病毒载体激活宿主炎症反应和调节信号转导途径已在先前文献中记载，包括MAP激酶和磷脂酰肌醇3-激酶（PI3-激酶）的活化。尚未检测到腺病毒载体激活这些途径对细胞存活的影响。 PI3-激酶/ Akt和ERK / MAP激酶信号通路均与细胞存活率相关。已经发现Akt通过其对凋亡相关蛋白的下游作用而在细胞存活和凋亡中起作用。 PI3-激酶或Akt的组成性激活可阻止c-Myc，紫外线辐射，转化生长因子-β，Fas和呼吸道合胞病毒感染引起的凋亡。我们检查了腺病毒载体感染对这些生存途径的激活及其下游后果的影响。用含有非特异性转基因，由巨细胞病毒启动子驱动的绿色荧光蛋白或无转基因的空载体的复制缺陷型腺病毒载体转导气道上皮细胞。然后将他们暴露于促细胞凋亡的放线菌素D加TNF-α，并评估细胞凋亡的证据。与仅用放线菌素/ TNF处理的细胞相比，感染了腺病毒载体的细胞凋亡减少了50％。当我们检查病毒载体感染细胞中生存途径ERK和AKT的诱导时，我们发现Akt和ERK均被激活。

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