...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Brain research >Exosomal miR-199a-5p derived from endothelial cells attenuates apoptosis and inflammation in neural cells by inhibiting endoplasmic reticulum stress
【24h】

Exosomal miR-199a-5p derived from endothelial cells attenuates apoptosis and inflammation in neural cells by inhibiting endoplasmic reticulum stress

机译：通过抑制内质网应力，源自内皮细胞的外泌体miR-199a-5p衍生自内皮细胞中神经细胞中的凋亡和炎症

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

Remote ischemic post-conditioning (RIPostC) is a technique that can protect vital organs in an indirect manner, the effects of which are exerted by the long-distance exosome-mediated transfer of functional factors. In the current study, the possible mechanism driving the function of RIPostC was explored using an in vitro system by focusing on miR-199a-5p and its downstream effectors involved in endoplasmic reticulum (ER) stress. Human umbilical vein endothelial cells (HUVECs) were administrated with hypoxia/re-oxygenation (H/R) process and exosomes were collected from the H/R-treated HUVECs. The levels of miR-199a-5p in HUVECs and exosomes were detected. Afterwards, H/R-treated SH-SY5Y neural cells was incubated with H/R HUVEC-derived exosomes, and the effect on cell apoptosis, inflammation, and miR-199a-5p-mediated ER stress was assessed. Furthermore, the key role of miR-199a-5p suppression in the protection effect of HUVEC-derived exosomes was validated by transfecting neural cells with specific inhibitor. The results showed that H/R administration increased miR-199a-5p levels both in HUVECs and exosomes. The incubation of neural cells with exosomes suppressed cell apoptosis and inflammation, and induced the level of miR-199a-5p, which led to suppressed ER stress. Moreover, the transfection of miR-199a-5p inhibitor blocked the anti-H/R function of exosomes. Taken together, the findings outlined in the current study showed that the protection effect of HUVEC derived miR-199a-5p on neural cells was exerted via exosome transfer, which then suppressed the ER stress-induced apoptosis and inflammation by targeting BIP.
机译：远程缺血后调节（RIPOSTC）是一种能够以间接方式保护重要器官的技术，其效果是通过长距离外出介导的功能因子的转移来施加的效果。在目前的研究中，通过专注于MIR-199A-5P及其下游效应器，通过体外系统探索驱动RIPOSTC功能的可能机制，并涉及内质网（ER）应力的下游效应。人的脐静脉内皮细胞（HUVEC）施用缺氧/重新氧合（H / R）过程，从H / R处理的Huvecs收集外泌体。检测到Huvecs和外泌体中miR-199a-5p的水平。然后，将H / R处理的SH-SE5Y神经细胞与H / R Huvec衍生的外来体一起孵育，评估对细胞凋亡，炎症和miR-199A-5P介导的ER应激的影响。此外，通过用特异性抑制剂转染神经细胞来验证miR-199a-5p抑制在Huvec衍生的外泌体保护作用中的关键作用。结果表明，H / R管理在HUVECS和外泌体中增加了MIR-199A-5P水平。用外来体培养神经细胞抑制细胞凋亡和炎症，并诱导MIR-199A-5P的水平，导致抑制ER应激。此外，miR-199A-5P抑制剂的转染阻断外泌体的抗H / R函数。在一起，目前的研究中概述的研究结果表明，通过外出转移施加Huvec衍生的MiR-199A-5P对神经细胞的保护作用，然后通过靶向BIP抑制ER应激诱导的凋亡和炎症。

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