Research Paper Volume 12, Issue 24 pp 26188—26198
MiR-223/NFAT5 signaling suppresses arterial smooth muscle cell proliferation and motility in vitro
- 1 Department of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi’an 710038, Shaanxi, China
- 2 Department of Cardiology, Air Force General Hospital, PLA, Beijing 100142, China
- 3 Department of Cardiology, PLA Army General Hospital, Beijing 100700, China
- 4 Department of Cardiology, Beijing Chest Hospital Heart Center, Capital Medical University, Beijing 101149, China
- 5 Division of Cardiology, Second Affiliated Hospital of Xi’an Jiao Tong University, Xi’an 710004, Shaanxi, China
Received: November 2, 2019 Accepted: October 31, 2020 Published: December 28, 2020https://doi.org/10.18632/aging.202395
How to Cite
Copyright: © 2020 Su 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.
Aberrant proliferation and migration of vascular smooth muscle cells contributes to cardiovascular diseases (CVDs), including atherosclerosis. MicroRNA-223 (miR-223) protects against atherosclerotic CVDs. We investigated the contribution of miR-223 to platelet-derived growth factor-BB (PDGF-BB)-induced proliferation and migration of human aortic smooth muscle cells (HASMCs). We found that miR-223 was downregulated in PDGF-BB-treated HASMCs in a dose- and time-dependent manner, while nuclear factor of activated T cells 5 (NFAT5) was upregulated. Gain- and loss-of-function studies demonstrated that miR-223 treatment reduced PDGF-BB-induced HASMC proliferation and motility, whereas miR-223 inhibitor enhanced these processes. Moreover, NFAT5 was identified as a direct target of miR-223 in HASMC. The inhibitory effects of miR-223 on HASMC proliferation and migration were partly rescued by NFAT5 restoration. Overall, these findings suggest that miR-223 inhibits the PDGF-BB-induced proliferation and motility of HASMCs by targeting NFAT5 and that miR-223 and NFAT5 may be potential therapeutic targets for atherosclerosis.