lncRNA GAPLINC regulates vascular endothelial cell apoptosis in atherosclerosis
Introduction In this study, we investigated the role of the long non-coding RNA GAPLINC in atherosclerosis under oxidized low-density lipoprotein (ox-LDL) treatment. Material and methods We utilized ox-LDL exposed human aortic endothelial cells as an in-vitro model. The expression level of GAPLINC...
Main Authors: | , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Termedia Publishing House
2023-07-01
|
Series: | Archives of Medical Science |
Subjects: | |
Online Access: | https://www.archivesofmedicalscience.com/lncRNA-GAPLINC-regulates-vascular-endothelial-cell-apoptosis-in-atherosclerosis,169383,0,2.html |
Summary: | Introduction
In this study, we investigated the role of the long non-coding RNA GAPLINC in atherosclerosis under oxidized low-density lipoprotein (ox-LDL) treatment.
Material and methods
We utilized ox-LDL exposed human aortic endothelial cells as an in-vitro model. The expression level of GAPLINC was quantified by qPCR in different times and concentrations of ox-LDL treatment conditions. Cell apoptosis rate and cell cycle profiles were assessed by flow cytometry and TUNEL assay. The target association was confirmed using a luciferase reporter assay and Western blot.
Results
We found that GAPLINC expression was induced by ox-LDL treatment, but cell proliferation ability was significantly inhibited. We further confirmed that overexpressing of lncRNA GAPLINC in ox-LDL-exposed HAECs decreased cell proliferation by increasing cell apoptosis and arresting cell cycle in G2/M and S phase. Importantly, the detailed mechanistic analysis elucidated that LncRNA GAPLINC acts as a decoy to sequester miR-183-5p to prevent it from binding to target PDCD4. MiR-183-5p targets GAPLINC, and PDCD4 is a downstream target of miR-183-5p, and the cellular effects of this direct interaction were confirmed by a rescue assay experiment.
Conclusions
The present study demonstrates that upregulation of lncRNA GAPLINC represses the binding of miR-183-5p to the PDCD4 promoter region and then promotes PDCD4 expression, thereby inducing cell apoptosis and suppressing endothelial cell proliferation. |
---|---|
ISSN: | 1734-1922 1896-9151 |