首页> 美国卫生研究院文献>Aging (Albany NY) >The long noncoding RNA HCG18 participates in PM2.5-mediated vascular endothelial barrier dysfunction
【2h】

The long noncoding RNA HCG18 participates in PM2.5-mediated vascular endothelial barrier dysfunction

机译:长的非编码RNA HCG18参与PM2.5介导的血管内皮阻隔功能障碍

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Increased vascular endothelial permeability can disrupt vascular barrier function and further lead to multiple human diseases. Our previous reports indicated that particulate matter 2.5 (PM2.5) can enhance the permeability of vascular endothelial cells. However, the regulatory mechanism was not comprehensively demonstrated. Therefore, this work elucidated this mechanism by demonstrating that PM2.5 can increase the permeability of HUVECs by inhibiting the expression of Hickson compact group 18 (HCG18). Moreover, we demonstrated that lncRNA HCG18 functioned as a ceRNA for miR-21-5p and led to the derepression of its target SOX7, which could further transcriptionally activate the expression of VE-cadherin to regulate the permeability of HUVECs. In this study, we provide evidence that HCG18/miR-21-5p/SOX7/VE-cadherin signaling is involved in PM2.5-induced vascular endothelial barrier dysfunction.
机译:增加的血管内皮渗透性可以破坏血管阻隔功能并进一步导致多种人类疾病。我们以前的报道表明,颗粒物质2.5(PM2.5)可以增强血管内皮细胞的渗透性。但是,监管机制没有全面地证明。因此,通过证明PM2.5可以通过抑制Hickson Compact组18(HCG18)的表达来增加Huvecs的渗透性来阐明该机制。此外,我们证明了LNCRNA HCG18用作MIR-21-5P的CERNA,并导致其靶SOX7的DERELAGING,这可以进一步转录激活Ve-Cadherin的表达来调节HUVEC的渗透性。在这项研究中,我们提供了证据表明HCG18 / miR-21-5P / SOX7 / Ve-Cadherin信号传导参与PM2.5诱导的血管内皮屏障功能障碍。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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