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, 2020
https://doi.org/10.18632/aging.202395How to Cite
Abstract
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.