Research Paper Volume 13, Issue 10 pp 14159—14169
Silencing lncRNA AK136714 reduces endothelial cell damage and inhibits atherosclerosis
- 1 Department of Geriatrics, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
- 2 Department of Nursing, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
- 3 Department of Scientific Research and Education, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
- 4 Department of Stomatology, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
- 5 Department of Dynamic electrocardiogram, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
- 6 Department of Breast, The Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
Received: September 25, 2020 Accepted: April 2, 2021 Published: May 18, 2021
https://doi.org/10.18632/aging.203031How to Cite
Copyright: © 2021 Bai 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
Atherosclerosis correlates with ischemic cardio-cerebrovascular diseases such as coronary heart disease. Long non-coding RNAs (lncRNAs) can promote atherosclerosis. We investigated the role of the lncRNA AK136714 in atherosclerosis. Compared with the healthy group, lncRNA AK136714 expression was elevated in the plaque and plasma of the atherosclerosis patients in a GEO dataset. AK136714 silencing inhibited atherosclerosis formation in ApoE-/- mice. AK136714 silencing also protected the endothelial barrier and inhibited endothelial cell inflammation. In vitro assays showed that knockdown of AK136714 suppressed the inflammatory response and apoptosis in human umbilical vein endothelial cells (HUVECs). Moreover, AK136714 was found to bind directly to HuR to increase the mRNA stability of TNF-α, IL-1β and IL-6 mRNAs. In addition, AK136714 promoted the transcription of Bim. This study expands our understanding of the role of lncRNA AK136714 in atherosclerosis and provides potential drug targets for the treatment of atherosclerosis.