Aging
Navigate
Submit an Article
Research Paper|Volume 12, Issue 23|pp 23960—23973

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

Shiwen Wang1, Yuyin Lin1, Yue Zhong1, Maozhou Zhao1, Wei Yao4, Xiaohui Ren5, Qin Wang7, Xiaolan Guo1, Qian-Qian Zhang3, Jianwei Dai1,2,6
  • 1GMU-GIBH Joint School of Life Sciences, Center of Reproductive Medicine, Third Affiliated Hospital, Guangzhou Medical University, Guangzhou 510182, China
  • 2The State Key Lab of Respiratory Disease, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou 510120, China
  • 3Vascular Biology Research Institute, School of Basic Course, Guangdong Pharmaceutical University, Guangzhou 510006, China
  • 4Healthcare Department, Agency for Offices Administration, Haidian District, Beijing 100082, China
  • 5Ocean College of Hebei Agricultural University, Qinhuangdao 066003, China
  • 6Key Laboratory for Reproductive Medicine of Guangdong Province, Key Laboratory for Major Obstetric Disease of Guangdong Province, Key Laboratory of Reproduction and Genetics of Guangdong Higher Education Institutes, Third Affiliated Hospital of Guangzhou Medical University, Guangzhou 510150, China
  • 7National Institute of Environmental Health, Chinese Center for Disease Control and Prevention, Beijing 100021, China
* Equal contribution
Received: June 9, 2020Accepted: August 8, 2020Published: November 16, 2020
https://doi.org/10.18632/aging.104073

Copyright: © 2020 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.