Research Paper Volume 12, Issue 10 pp 8913—8922
HIX003209 promotes vascular smooth muscle cell migration and proliferation through modulating miR-6089
- 1 Department of Emergency, Tianjin First Center Hospital, Tianjin 300192, People’s Republic of China
- 2 Department of Physiology, School of Basic Medicine, Jinzhou Medicine University, Jinzhou 121000, Liaoning, People’s Republic of China
- 3 Clinical Nutrition Department, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, People’s Republic of China
- 4 Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba 3050005, Japan
- 5 Department of Anatomy, Dalian Medical University, Dalian 116044, Liaoning, People’s Republic of China
- 6 Department of Vascular Surgery, Dalian University Affiliated Xinhua Hospital, Dalian 116021, Liaoning, People’s Republic of China
- 7 Department of General Surgery, The First Affiliated Hospital, Dalian Medical University, Dalian 116011, Liaoning, People’s Republic of China
- 8 Department of Vascular Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, People’s Republic of China
- 9 Neurosurgery Department, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, People’s Republic of China
Received: October 23, 2019 Accepted: March 24, 2020 Published: May 27, 2020
https://doi.org/10.18632/aging.103079How to Cite
Copyright © 2020 Shi 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
Accumulating references have showed that long noncoding RNAs (lncRNAs) act important roles in the development of human diseases. The role and expression of HIX003209 remains unclear in the pathogenesis of atherosclerosis. We showed that HIX003209 expression was upregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. HIX003209 was overexpressed in vascular smooth muscle cells (VSMCs) induced by inflammatory mediators including tumor necrosis factor-α(TNF-α), ox-LDL and latelet-derived growth factor-BB (PDGF-BB). Ectopic expression of HIX003209 enhanced cell growth and migration and induced inflammatory mediators secretion such as interleukin 6 (IL-6), TNF-α and IL-1β in VSMCs. Furthermore, we showed that miR-6089 was downregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. There was a negative association between expression of HIX003209 and miR-6089 in atherosclerotic coronary tissues. MiR-6089 expression was decreased in VSMCs induced by inflammatory mediators including TNF-α, ox-LDL and PDGF-BB. Dual luciferase analysis showed that miR-6089 overexpression decreased luciferase activity of HIX003209 WT-type 3’-UTR but not the mut-type 3’-UTR. Overexpression of HIX003209 suppressed the expression of miR-6089 in VSMCs. Ectopic expression of HIX003209 induced cell growth, migration and the secretion of inflammatory mediators via regulating miR-6089 expression. These data suggested that HIX003209 promoted VSMCs proliferation, migration and the secretion of inflammatory mediators partly via regulating miR-6089.