...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of cellular physiology. >Inhibition of microRNA-103 attenuates inflammation and endoplasmic reticulum stress in atherosclerosis through disrupting the PTEN-mediated MAPK signaling
【24h】

Inhibition of microRNA-103 attenuates inflammation and endoplasmic reticulum stress in atherosclerosis through disrupting the PTEN-mediated MAPK signaling

机译：抑制微rna - 103变弱炎症内质网应激动脉粥样硬化通过扰乱PTEN-mediated MAPK信号

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

Atherosclerosis (AS), a chronic disorder of large arteries, is the underlying pathological process of heart disease and stroke. Former researchers have found that microRNAs (miRs) are involved in the several key processes of AS. Apolipoprotein E knockout (ApoE~(-/-)) mice fed a high-fat-diet (HFD) to establish AS model. The expression of miR-103 was characterized in the mice model. The effects of miR-103 on inflammation and endoplasmic reticulum stress (ERS) were analyzed when the expression of miR-103 was inhibited in ApoE~(-/-) mice fed an HFD and human aortic endothelial cells (HAECs) exposed to oxidized low-density lipoprotein (ox-LDL). The relationship between miR-103 and phosphatase and tensin homolog (PTEN) was identified by luciferase activity detection and real-time quantitative polymerase chain reaction (RT-qPCR). Gain- and loss-function approaches were further applied for investigating the regulatory effects of miR-103 and PTEN on ERS. Role of MAPK signaling was then analyzed using PD98059 to block this pathway. miR-103 was highly expressed in the ApoEApoE~(-/-) mice fed an HFD. Downregulation of miR-103 suppressed inflammation and ERS in endothelial cells isolated from ApoE~(-/-) mice fed a HFD and ox-LDL-exposed HAECs. In addition, miR-103 can target PTEN and downregulate its expression. Overexpression of PTEN reversed the miR-103-induced activation of MAPK signaling. Moreover, PTEN upregulation or MAPK signaling inhibition ease miR-103-induced inflammation and ERS in vivo and in vitro. Thus, miR-103 depletion restrains the progression of AS through blocking PTEN-mediated MAPK signaling.
机译：动脉粥样硬化(AS)的慢性疾病动脉,是潜在的病理过程心脏病和中风。发现小分子核糖核酸(大鹏)参与的几个关键过程。击倒(ApoE ~(- / -))老鼠的雌性后代(HFD)建立模型。mir - 103为特征的小鼠模型。mir - 103对炎症的影响内质网应激(ERS)进行了分析当mir - 103的表达被抑制载脂蛋白e ~(- / -)小鼠喂食HFD和人类主动脉内皮细胞(HAECs)暴露于氧化低密度脂蛋白(ox-LDL)。mir - 103和磷酸酶和之间的关系tensin同族体(PTEN)被发现荧光素酶活性检测和实时定量聚合酶链反应(RT-qPCR)。进一步获得和损失函数方法申请调查的监管效果mir - 103和PTEN的人。信号是使用PD98059分析阻止这个途径。ApoEApoE ~(- / -)小鼠喂食HFD。Downregulation mir - 103抑制炎症和人内皮细胞分离载脂蛋白e ~(- / -)小鼠喂食HFD ox-LDL-exposedHAECs。其表达下调。PTEN逆转mir - 103诱导激活MAPK信号。MAPK信号抑制缓解mir - 103诱导炎症和人体内和体外。mir - 103损耗控制的发展通过阻断PTEN-mediated MAPK信号。

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