Research Paper Advance Articles pp 23960—23973
The long noncoding RNA HCG18 participates in PM2.5-mediated vascular endothelial barrier dysfunction
- 1 GMU-GIBH Joint School of Life Sciences, Center of Reproductive Medicine, Third Affiliated Hospital, Guangzhou Medical University, Guangzhou 510182, China
- 2 The State Key Lab of Respiratory Disease, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou 510120, China
- 3 Vascular Biology Research Institute, School of Basic Course, Guangdong Pharmaceutical University, Guangzhou 510006, China
- 4 Healthcare Department, Agency for Offices Administration, Haidian District, Beijing 100082, China
- 5 Ocean College of Hebei Agricultural University, Qinhuangdao 066003, China
- 6 Key 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
- 7 National Institute of Environmental Health, Chinese Center for Disease Control and Prevention, Beijing 100021, China
Received: June 9, 2020 Accepted: August 8, 2020 Published: November 16, 2020https://doi.org/10.18632/aging.104073
How to Cite
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.
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.
lncRNA HCG18: Long non-coding RNA, HCG18; PM2.5: Particulate Matter 2.5; ceRNA: competing endogenous RNA; HUVECs: Human umbilical vein endothelial cells.