Research Paper Volume 12, Issue 13 pp 12684—12702
Silencing of long non-coding RNA Sox2ot inhibits oxidative stress and inflammation of vascular smooth muscle cells in abdominal aortic aneurysm via microRNA-145-mediated Egr1 inhibition
- 1 Department of Cardiovascular Surgery, Provincial Clinical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou 350001, P.R. China
- 2 Department of Cardiology, Provincial Clinical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou 350001, P.R. China
- 3 Department of Imaging, Provincial Clinical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou 350001, P.R. China
Received: September 26, 2019 Accepted: March 29, 2020 Published: July 6, 2020https://doi.org/10.18632/aging.103077
How to Cite
Copyright © 2020 Lin 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.
Long non-coding RNAs (lncRNAs) have been largely reported to contribute to the development and progression of abdominal aortic aneurysm (AAA), a common vascular degenerative disease. The present study was set out with the aim to investigate the possible role of lncRNA Sox2ot in the development of AAA. In this study, we found that lncRNA Sox2ot and early growth response factor-1 (Egr1) were highly expressed, while microRNA (miR)-145 was poorly expressed in Ang II-induced AAA mice and oxidative stress-provoked vascular smooth muscle cell (VSMC) model. Egr1 was a potential target gene of miR-145, and lncRNA Sox2ot could competitively bind to miR-145 to upregulate Egr1 expression. Overexpression of miR-145-5p was found to attenuate oxidative stress and inflammation by inhibiting Egr1 both in vivo and in vitro, which was counteracted by lncRNA Sox2ot. Taken together, the present study provides evidence that downregulation of lncRNA Sox2ot suppressed the expression of Egr1 through regulating miR-145, thus inhibiting the development of AAA, highlighting a theoretical basis for AAA treatment.