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OIP5-AS1的下调通过调节MiR-145-5p/ROCK1轴抑制心肌缺血/再灌注损伤中的细胞凋亡。

Downregulation of OIP5-AS1 inhibits apoptosis in myocardial ischemia/reperfusion injury via modulating the MiR-145-5p/ROCK1 axis.

作者信息

Yang Jingyan, Liu Jing, Liu Xiaobo, Xu Dongling, Zhang Juan

机构信息

Department of Pathology, The Second Hospital of Shandong University, Jinan, Shandong Province, China.

Department of Cardiology, The Second Hospital of Shandong University, Jinan, Shandong Province, China.

出版信息

PLoS One. 2025 May 20;20(5):e0324909. doi: 10.1371/journal.pone.0324909. eCollection 2025.

DOI:10.1371/journal.pone.0324909
PMID:40392837
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12091815/
Abstract

PURPOSE

The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was conducted with the objective of investigating the function of OIP5-AS1 in myocardial I/R injury and exploring its potential mechanisms.

METHODS

In order to simulate the conditions of I/R, H9c2 cells were cultured in hypoxic/reoxygenated environments. Induction of I/R in Sprague-Dawley rats was achieved by ligating the left anterior descending coronary artery for 30 minutes followed by 180 minutes of reperfusion. OIP5-AS1 expression levels were assessed, and the degree of apoptosis was evaluated by TUNEL staining. Bioinformatic analysis was conducted to predict the interaction between microRNA-145-5p (miR-145-5p) and OIP5-AS1, and the expression levels of miR-145-5p and ROCK1 were determined.

RESULTS

Elevated levels of OIP5-AS1 were observed in H/R-treated H9c2 cells and in rat I/R models. Elevated OIP5-AS1 expression was associated with an increased incidence of apoptosis. The silencing of OIP5-AS1 in I/R conditions resulted in a significant suppression of cell apoptosis, reduced cleavage of caspase-3, decreased Bax levels, and increased Bcl-2 levels. Bioinformatic analysis predicted binding sites between miR-145-5p and OIP5-AS1. Furthermore, depletion of OIP5-AS1 in I/R conditions resulted in a substantial increase in miR-145-5p expression and a decrease in ROCK1 expression. The suppression of miR-145-5p reversed the effects of OIP5-AS1 depletion in I/R conditions.

CONCLUSIONS

Downregulation of OIP5-AS1 may prevent apoptosis in myocardial I/R injury by modulating the miR-145-5p/ROCK1 axis.

摘要

目的

长链非编码RNA OIP5-AS1在心肌缺血/再灌注（I/R）损伤诱导的细胞凋亡中的作用仍有待充分阐明。本研究旨在探讨OIP5-AS1在心肌I/R损伤中的功能，并探索其潜在机制。

方法

为模拟I/R条件，将H9c2细胞置于缺氧/复氧环境中培养。通过结扎Sprague-Dawley大鼠左冠状动脉前降支30分钟，然后再灌注180分钟来诱导I/R。评估OIP5-AS1表达水平，并通过TUNEL染色评估细胞凋亡程度。进行生物信息学分析以预测微小RNA-145-5p（miR-145-5p）与OIP5-AS1之间的相互作用，并测定miR-145-5p和ROCK1的表达水平。

结果

在缺氧/复氧处理的H9c2细胞和大鼠I/R模型中观察到OIP5-AS1水平升高。OIP5-AS1表达升高与细胞凋亡发生率增加相关。在I/R条件下沉默OIP5-AS1可显著抑制细胞凋亡，减少半胱天冬酶-3的切割，降低Bax水平，并增加Bcl-2水平。生物信息学分析预测了miR-145-5p与OIP5-AS1之间的结合位点。此外，在I/R条件下耗竭OIP5-AS1可导致miR-145-5p表达大幅增加，ROCK1表达降低。抑制miR-145-5p可逆转I/R条件下OIP5-AS1耗竭的作用。

结论

下调OIP5-AS1可能通过调节miR-145-5p/ROCK1轴预防心肌I/R损伤中的细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/fd3c96ffc51c/pone.0324909.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/15557ff4e07f/pone.0324909.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/b07b08598751/pone.0324909.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/22715c366132/pone.0324909.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/2afd604925c2/pone.0324909.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/82c53bf1b556/pone.0324909.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/9eea7e6d69d5/pone.0324909.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/95e2a2af679c/pone.0324909.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/34189d493060/pone.0324909.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/fd3c96ffc51c/pone.0324909.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/15557ff4e07f/pone.0324909.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/b07b08598751/pone.0324909.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/22715c366132/pone.0324909.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/2afd604925c2/pone.0324909.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/82c53bf1b556/pone.0324909.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/9eea7e6d69d5/pone.0324909.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/95e2a2af679c/pone.0324909.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/34189d493060/pone.0324909.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a5f/12091815/fd3c96ffc51c/pone.0324909.g009.jpg

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