Open AccessLong non‑coding RNA NEAT1 modulates hypoxia/reoxygenation‑induced cardiomyocyte injury via targeting microRNA‑520a
Author(s) -
HuaJun Wu,
Guanmin Tang,
Ping-yang Shao,
Hongxing Zou,
WeiFeng Shen,
MingDe Huang,
Hanghai Pan,
Chao Zhai,
Gang Qian
Publication year - 2019
Publication title -
experimental and therapeutic medicine
Language(s) - Uncategorized
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2019.7788
Subject(s) - apoptosis , microrna , downregulation and upregulation , gene knockdown , microbiology and biotechnology , chemistry , hypoxia (environmental) , flow cytometry , terminal deoxynucleotidyl transferase , cell , tunel assay , biology , biochemistry , gene , organic chemistry , oxygen
In the present study, a hypoxia/reoxygenation (H/R) model of cardiomyocytes was established to investigate the effects of long non-coding RNA (LncRNA) Nuclear Enriched Abundant Transcript 1 (NEAT1) and microRNA (miR)-520a on H/R-induced cardiomyocyte apoptosis. Flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling staining were used to evaluate cell apoptosis. Luciferase activity assay was used to investigate whether miR-520a targets NEAT1. Results revealed that NEAT1 was significantly upregulated and miR-520a was downregulated in the ischemia/reperfusion myocardium and the cardiomyocytes that received H/R treatment. Further study demonstrated that knockdown of NEAT1 and overexpression of miR-520a serves a protective role against H/R-induced cardiomyocyte apoptosis. miR-520a directly targets NEAT1 and its expression level is negatively correlated with that of NEAT1. The findings suggested that NEAT1 and miR-520a may protect cardiomyocytes from apoptosis through regulating apoptotic proteins B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein, and altering cleaved caspase3 expression levels.