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探讨长链非编码 RNA HOTAIR 对心肌缺血再灌注损伤诱导的细胞凋亡的影响。

Investigating the effect of lncRNA HOTAIR on apoptosis induced by myocardial ischemia-reperfusion injury.

机构信息

Department of Rehabilitation Medicine, The First People's Hospital of Tonglu, Tonglu County, Hangzhou, Zhejiang 311500, P.R. China.

School of Life Science, Huzhou University, Huzhou, Zhejiang 313000, P.R. China.

出版信息

Mol Med Rep. 2021 Mar;23(3). doi: 10.3892/mmr.2020.11808. Epub 2021 Jan 5.

DOI:10.3892/mmr.2020.11808
PMID:33398378
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7821281/
Abstract

The present study aimed to investigate the effect of the long non‑coding ribonucleic acid (lncRNA) HOX transcript antisense intergenic RNA (HOTAIR) on apoptosis induced by ischemia‑reperfusion injury. Differential lncRNAs in myocardial ischemia rats were screened by a lncRNA microarray and the expression levels of lncRNA HOTAIR and microRNA (miR)‑130a‑3p were analyzed using reverse transcription‑quantitative polymerase chain reaction in hypoxia‑induced cardiomyocytes. The mechanism of lncRNA HOTAIR in cardiotoxicity was investigated using cell transfection, lncRNA knockdown, Cell Counting Kit‑8, flow cytometry, western blotting, dual luciferase reporter assays and RNA immunoprecipitation. The expression level of lncRNA HOTAIR was significantly downregulated in the ischemic myocardium of rats. Overexpression of HOTAIR in H9c2 (rat cardiomyocyte line) cells could inhibit the apoptosis induced by H2O2. A direct interaction was found between HOTAIR and miR‑130a‑3p, and mouse double minute 4 (MDM4) was also found to be a potential target of miR‑130a‑3p. The overexpression of MDM4 in H9c2 cells transfected with miR‑130a‑3p mimics increased apoptosis, and miR‑130a‑3p targeted inhibition of MDM4 promoted H2O2‑induced apoptosis of H9c2 cells. Overall, HOTAIR was found to inhibit the apoptosis of H9c2 cells induced by H2O2 through the miR‑130a‑3p/MDM4 axis.

摘要

本研究旨在探讨长链非编码 RNA（lncRNA）HOX 转录反义基因间 RNA（HOTAIR）对缺血再灌注损伤诱导的细胞凋亡的影响。通过 lncRNA 微阵列筛选心肌缺血大鼠中的差异 lncRNA，并使用逆转录-定量聚合酶链反应分析缺氧诱导的心肌细胞中 lncRNA HOTAIR 和 microRNA（miR）-130a-3p 的表达水平。使用细胞转染、lncRNA 敲低、细胞计数试剂盒-8、流式细胞术、Western blot、双荧光素酶报告基因测定和 RNA 免疫沉淀法研究 lncRNA HOTAIR 在心脏毒性中的作用机制。lncRNA HOTAIR 在大鼠缺血心肌中的表达水平显著下调。在 H9c2（大鼠心肌细胞系）细胞中过表达 HOTAIR 可抑制 H2O2 诱导的细胞凋亡。发现 HOTAIR 与 miR-130a-3p 之间存在直接相互作用，并且还发现 mouse double minute 4（MDM4）是 miR-130a-3p 的潜在靶标。转染 miR-130a-3p 模拟物的 H9c2 细胞中 MDM4 的过表达增加了细胞凋亡，并且 miR-130a-3p 对 MDM4 的靶向抑制促进了 H2O2 诱导的 H9c2 细胞凋亡。总之，发现 HOTAIR 通过 miR-130a-3p/MDM4 轴抑制 H2O2 诱导的 H9c2 细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/a74fd39b46a7/mmr-23-03-11808-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/3487fea1207b/mmr-23-03-11808-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/03e07ee3bcf4/mmr-23-03-11808-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/5120cb12777f/mmr-23-03-11808-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/20b85cf65f92/mmr-23-03-11808-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/cda1db5681a1/mmr-23-03-11808-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/a74fd39b46a7/mmr-23-03-11808-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/3487fea1207b/mmr-23-03-11808-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/03e07ee3bcf4/mmr-23-03-11808-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/5120cb12777f/mmr-23-03-11808-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/20b85cf65f92/mmr-23-03-11808-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/cda1db5681a1/mmr-23-03-11808-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/7821281/a74fd39b46a7/mmr-23-03-11808-g05.jpg

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