Research Paper Volume 12, Issue 9 pp 8413—8422
LncRNA ILF3-AS1 mediated the occurrence of epilepsy through suppressing hippocampal miR-212 expression
- 1 Department of Neurology, The Sixth Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China
- 2 Department of Neurology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China
- 3 Department of Pathology, The Eight Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China
- 4 Department of Neurology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China
- 5 Department of Neurosurgery, Guangdong 999 Brain Hospital, Guangzhou, China
Received: July 15, 2019 Accepted: April 16, 2020 Published: May 13, 2020https://doi.org/10.18632/aging.103148
How to Cite
Copyright © 2020 Cai 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.
Increased expression of some matrix metalloproteinases (MMPs) is closely associated with epilepsy. However, factors that promote their expression have not been clarified. Long noncoding RNAs (lncRNAs) play crucial roles in the development of human diseases, including various cancers, but its potential function in temporal lobe epilepsy (TLE) has remained unexplored. In this study, we showed that hippocampal and serum ILF3-AS1 levels are higher in TLE patients than in matched controls. Interleukin (IL)-1β and tumor necrosis factor (TNF)-α induced ILF3-AS1 expression in astrocytes, while ectopic expression of ILF3-AS1 enhanced IL-6 and TNF-α expression. Ectopic ILF3-AS1 in astrocytes also increased expression of MMP2, MMP3, MMP9 and MMP14, but suppressed expression of miR-212. Consistent with that finding, miR-212 levels were lower in the hippocampus and serum of TLE patients than their controls. This suggests that ILF3-AS1 promotes expression of inflammatory cytokines and MMPs by targeting miR-212 and that ILF3-AS1 plays a crucial role in the development of TLE.