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Published on: June 15, 2018
LncRNA XIST promotes myocardial infarction by regulating FOS through targeting miR-101a-3p
Bin Lin1, Jing Xu1, Feng Wang1
1Department of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China.
Abstract:
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.
Insights
Long non-coding RNA XIST regulates cardiomyocyte apoptosis and myocardial infarction by targeting miR-101a-3p. Silencing XIST protects against myocardial infarction by reducing FOS expression and apoptosis.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) play crucial roles in cellular processes.
- X inactive specific transcript (XIST) is implicated in various biological functions.
- Cardiomyocyte apoptosis is a key event in myocardial infarction (MI).
Purpose of the Study:
- To investigate the role of lncRNA XIST in regulating cardiomyocyte apoptosis.
- To explore the potential mechanism involving miR-101a-3p and FOS.
- To assess the therapeutic potential of XIST modulation in myocardial infarction.
Main Methods:
- Neonatal mouse cardiomyocytes (NMCMs) subjected to anoxia.
- MTT assay and flow cytometry for proliferation and apoptosis.
- Bioinformatic analysis, luciferase reporter, pull-down, and RNA immunoprecipitation assays.
- qRT-PCR and Western blot for gene and protein expression.
- Myocardial infarction (MI) mouse model.
Main Results:
- XIST expression was upregulated in NMCMs under anoxia.
- XIST sponged miR-101a-3p, leading to increased FOS expression.
- Silencing XIST improved cell viability and reduced apoptosis in vitro.
- XIST inhibition attenuated MI in vivo by decreasing c-FOS and apoptosis markers.
Conclusions:
- XIST promotes cardiomyocyte apoptosis and exacerbates myocardial infarction.
- The XIST/miR-101a-3p/FOS axis is critical in MI pathogenesis.
- Targeting XIST represents a potential therapeutic strategy for myocardial infarction.
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