...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Wound-induced p38MAPK-dependent histone H3 phosphorylation correlates with increased COX-2 expression in enterocytes.
【24h】

Wound-induced p38MAPK-dependent histone H3 phosphorylation correlates with increased COX-2 expression in enterocytes.

机译：Wound-induced p38MAPK-dependent组蛋白H3磷酸化与cox - 2的增加肠上皮细胞的表达。

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

Gastrointestinal epithelial cell damage triggers an important biological response called restitution, a process aimed at re-epithelializing the wounded areas. Unfortunately, little is known about the intrinsic molecular signaling events implicated in this host response. We hypothesized that wounding intestinal epithelial cells activates signaling pathways leading to chromatin modification and COX-2 upregulation during restitution. Confluent rat IEC18 cells were mechanically wounded by multiple parallel scratches using a pipet tip. NF-kappaB(Ser536), p38, and histone H3(Ser10) (H3S10) phosphorylation were determined by Western blot using specific phospho-antibodies. COX-2 gene expression was evaluated by RT-PCR, Western Blot, and ELISA. Association of phosphorylated H3, RelA (NF-kappaB), and RNA polymerase II to the COX-2 gene promoter was evaluated by chromatin immunoprecipitation (ChIP). The specific inhibitors Bay11-7082 and SB239063 as well as Ad5IkappaB-superrepressor (Ad5IkappaBAA) and Ad5dnp38 were used to block NF-kappaB- and p38-signaling pathways, respectively. Wounding induced a rapid and sustained (24 h) phosphorylation of RelAS536, H3S10, and p38MAPK in enterocytes. ChIP analysis of the COX-2 gene promoter demonstrated the presence of phospho-H3S10 and recruitment of RelA and RNA polymerase II, a process blocked by SB239063. Finally, molecular blockade of NF-kappaB (Ad5IkappaBAA) or p38MAPK (Ad5dnp38) signaling strongly inhibited enterocyte restitution. p38MAPK-dependent histone 3 phosphorylation is an important component of the intestinal wound-healing response. Targeting-signaling pathways selectively involved in healing/restitution may provide a novel means to maintain or re-establish host intestinal barrier integrity.
机译：胃肠道上皮细胞损伤的诱因一个重要的生物反应赔偿,这一过程旨在re-epithelializing受伤的区域。不幸的是,人们很少知道内在的分子信号事件有牵连在这个主机响应。伤害肠道上皮细胞激活信号通路导致染色质修改和cox - 2 upregulation归还。由多个并行机械地受伤划痕用移液管小费。p38和组蛋白H3 (Ser10) (H3S10)磷酸化是由蛋白质印迹使用特定phospho-antibodies。表达式是评估通过rt - pcr、免疫印迹和ELISA。(NF-kappaB)和RNA聚合酶II cox - 2基因启动子是由染色质评估免疫沉淀反应(芯片)。抑制剂bay11 - 7082和SB239063以及Ad5dnp38被用来阻止NF-kappaB,分别p38-signaling通路。诱导一个快速和持续(24小时)的磷酸化RelAS536、H3S10 p38MAPK在肠上皮细胞。启动子的存在phospho-H3S10 RelA和RNA和招聘聚合酶II,一个被SB239063过程。最后,分子NF-kappaB的封锁强烈抑制肠上皮细胞恢复。p38MAPK-dependent 3组蛋白磷酸化是一个肠道的重要组成部分愈合反应。途径有选择地参与治疗/赔偿可能提供一个新的手段维持或恢复宿主肠道屏障的完整性。

著录项

相似文献

  • 外文文献
  • 中文文献
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