Research Paper Volume 12, Issue 8 pp 7232—7247
LncRNA XIST promotes myocardial infarction by regulating FOS through targeting miR-101a-3p
- 1 Department of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China
received: June 12, 2019 ; accepted: March 24, 2020 ; published: April 21, 2020 ;https://doi.org/10.18632/aging.103072
How to Cite
Copyright © 2020 Lin 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.
The purpose of this study was to reveal the hypothesis that lncRNA X inactive specific transcript (XIST) can participate in the regulation of cardiomyocyte apoptosis in neonatal mice cardiomyocytes (NMCMs) and myocardial infarction (MI) through targeting miR-101a-3p. NMCMs were isolated from neonatal C57BL/6 mice and anoxia was induced in hypoxic chamber. MTT assay and flow cytometry were used to determine proliferation and apoptosis respectively. The target relationship among XIST, miR-101a-3p and FOS was revealed by bioinformatic analysis, luciferase reporter assay, pull-down assay and RNA immunoprecipitation assay. The expression of XIST, miR-101a-3p, FOS and apoptosis-related proteins was determined by qRT-PCR or western blot. MI model was constructed to reveal the role of XIST. We found that XIST was up-regulated in NMCMs under anoxia condition. Moreover, XIST increased FOS expression by sponging miR-101a-3p in anoxia cells. Silencing XIST expression improved cell viability and suppressed apoptosis in vitro and inhibited myocardial infarction by reducing the level of c-FOS and apoptosis-related proteins in vivo. Our findings suggest that XIST is involved in MI, modulation of its level can be used as a new strategy or potential target in the treatment of myocardial infarction.