Aging
Navigate
Submit an Article
Research Paper|Volume 13, Issue 10|pp 14159—14169

Silencing lncRNA AK136714 reduces endothelial cell damage and inhibits atherosclerosis

Jing Bai1, Jianxia Liu2, Zexian Fu3, Yuanyuan Feng4, Bing Wang5, Wenjuan Wu6, Ruiying Zhang1
  • 1Department of Geriatrics, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
  • 2Department of Nursing, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
  • 3Department of Scientific Research and Education, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
  • 4Department of Stomatology, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
  • 5Department of Dynamic electrocardiogram, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
  • 6Department of Breast, The Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
Received: September 25, 2020Accepted: April 2, 2021Published: May 18, 2021
https://doi.org/10.18632/aging.203031

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.