• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Microbial Pathogenesis >lncRNA TUG1 regulates ulcerative colitis through miR-142-5p/SOCS1 axis
【24h】

lncRNA TUG1 regulates ulcerative colitis through miR-142-5p/SOCS1 axis

机译：LNCRNA Tug1通过MiR-142-5P / SOCS1轴调节溃疡性结肠炎

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

Ulcerative colitis (UC) is a long-lasting inflammation disease which finally results in ulcer of the colon and rectum. The long non-coding RNA (lncRNA) TUG1 has been described to target miR-142 and regulate its expression. In current study, we evaluated the effects of long non-coding RNA TUG1 on cell injury and inflammatory cytokine production using a TNF alpha-treated HT-29 cells model. We monitored the level of TUG1 in colonic mucosa tissue of UC patients and in TNF-alpha-treated HT-29 cells. We investigated the effects of TUG1 on miR-142-5p and SOCS1 expression, cell viability, lactate dehydrogenase (LDH) release, production of nitrite and PGE2 after TNF-alpha treatment in HT-29 cells. We also investigated the effects of TUG1 on TNF-alpha-induced IL-6, IL-8 and IL-1 beta expression in HT-29 cells. We detected down-regulated TUG1 level in colonic mucosa tissue of UC patients and in TNF-alpha-treated HT-29 cells. Overexpression of TUG1 enhanced cell viability, decreased LDH release, decreased nitrite and PGE2 production after TNF-alpha treatment in HT-29 cells. TUG1 prevented IL-1 beta, IL-6 and IL-8 production in TNF-alpha-treated cells. TUG1 targeted miR-142-5p and inhibited its expression while enhanced SOCS1 expression. Overexpression of miR-142-5p abolished TUG1-mediated inhibition of TNF-induced inflammatory cytokines production. TUG1 negatively regulated inflammation in ulcerative colitis through miR142-5p/SOCS1 axis.
机译：溃疡性结肠炎（UC）是一种持久的炎症疾病，最终导致结肠和直肠的溃疡。已经描述了长的非编码RNA（LNCRNA）Tug1靶向miR-142并调节其表达。在目前的研究中，我们使用TNFα处理的HT-29细胞模型评估了长期非编码RNA TNA Tug1对细胞损伤和炎症细胞因子产生的影响。我们监测了UC患者的结肠粘膜组织和TNF-α处理的HT-29细胞的Tug1水平。我们研究了TNF-α在HT-29细胞中TNF-α处理后对MIR-142-5P和SOCS1表达，细胞活力，乳酸脱氢酶（LDH）释放，亚硝酸盐和PGE2的影响的影响。我们还研究了Tug1对HT-29细胞中TNF-α诱导的IL-6，IL-8和IL-1β表达的影响。我们在UC患者的结肠粘膜组织和TNF-α处理的HT-29细胞中检测到下调的Tug1水平。 Tug1增强细胞活力的过表达增强，降低LDH释放，在HT-29细胞中的TNF-α处理后降低亚硝酸盐和PGE2产生。 Tug1预防IL-1β，IL-6和IL-8在TNF-α处理的细胞中产生。 Tug1针对miR-142-5p并抑制了它的表达，同时增强了SOCS1表达。 MIR-142-5P的过表达废除了Tug1介导的TNF诱导的炎性细胞因子产生的抑制作用。 Tug1通过MiR142-5P / SOCS1轴对溃疡性结肠炎产生负面调节炎症。

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