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长链非编码 RNA PINK1-AS 通过海绵吸附 miR-203 调控 ATF2 加重脑缺血/再灌注氧化应激损伤

lncRNA PINK1-AS Aggravates Cerebral Ischemia/Reperfusion Oxidative Stress Injury through Regulating ATF2 by Sponging miR-203.

机构信息

The Affiliated Changsha Hospital of Hunan Normal University, Changsha, Hunan 410006, China.

College of Medicine, Hunan Normal University, Changsha, Hunan 410006, China.

出版信息

Oxid Med Cell Longev. 2022 Jul 9;2022:1296816. doi: 10.1155/2022/1296816. eCollection 2022.

DOI:10.1155/2022/1296816
PMID:35855866
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9288285/
Abstract

Ischemic stroke is a common disease that led to high mortality and high disability. NADPH oxidase 2- (NOX2-) mediated oxidative stress and long noncoding RNA have important roles in cerebral ischemia/reperfusion (CI/R) injury, whereas whether there is interplay between them remains to be clarified. This study was performed to observe the role of lncRNA PINK1-antisense RNA (PINK1-AS) in NOX2 expression regulation. An in vivo rat model (MCAO) and an in vitro cell model (H/R: hypoxia/reoxygenation) were utilized for CI/R oxidative stress injury investigation. The expression levels of lncRNA PINK1-AS, activating transcription factor 2 (ATF2), NOX2, and caspase-3 and the production level of ROS and cell apoptosis were significantly increased in CI/R injury model rats or in H/R-induced SH-SY5Y cells, but miR-203 was significantly downregulated. There was positive correlation between PINK1-AS expression level and ROS production level. PINK1-AS and ATF2 were found to be putative targets of miR-203. Knockdown of lncRNA PINK1-AS or ATF2 or the overexpression of miR-203 significantly reduced oxidative stress injury via inhibition of NOX2. Overexpression of lncRNA PINK1 significantly led to oxidative stress injury in SH-SY5Y cells through downregulating miR-203 and upregulating ATF2 and NOX2. lncRNA PINK1-AS and ATF2 were the targets of miR-203, and the lncRNA PINK1-AS/miR-203/ATF2/NOX2 axis plays pivotal roles in CI/R injury. Therefore, lncRNA PINK1-AS is a possible target for CR/I injury therapy by sponging miR-203.

摘要

缺血性脑卒中是一种常见的疾病，导致高死亡率和高残疾率。NADPH 氧化酶 2-（NOX2-）介导的氧化应激和长链非编码 RNA 在脑缺血/再灌注（CI/R）损伤中具有重要作用，然而它们之间是否存在相互作用仍有待阐明。本研究旨在观察长链非编码 RNA PINK1-反义 RNA（PINK1-AS）在 NOX2 表达调控中的作用。采用体内大鼠模型（MCAO）和体外细胞模型（H/R：缺氧/复氧）研究 CI/R 氧化应激损伤。在 CI/R 损伤模型大鼠或 H/R 诱导的 SH-SY5Y 细胞中，lncRNA PINK1-AS、激活转录因子 2（ATF2）、NOX2、caspase-3 的表达水平以及 ROS 的产生水平和细胞凋亡明显增加，但 miR-203 明显下调。PINK1-AS 表达水平与 ROS 产生水平呈正相关。发现 PINK1-AS 和 ATF2 是 miR-203 的潜在靶标。敲低 lncRNA PINK1-AS 或 ATF2 或过表达 miR-203 可通过抑制 NOX2 显著减轻氧化应激损伤。过表达 lncRNA PINK1 可通过下调 miR-203 并上调 ATF2 和 NOX2 导致 SH-SY5Y 细胞发生氧化应激损伤。lncRNA PINK1-AS 和 ATF2 是 miR-203 的靶标，lncRNA PINK1-AS/miR-203/ATF2/NOX2 轴在 CI/R 损伤中起关键作用。因此，lncRNA PINK1-AS 可能通过海绵吸附 miR-203 成为 CR/I 损伤治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b5e/9288285/b07a817cf211/OMCL2022-1296816.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b5e/9288285/4265d8e6464b/OMCL2022-1296816.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b5e/9288285/5d6cfd55a700/OMCL2022-1296816.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b5e/9288285/c42b64048db9/OMCL2022-1296816.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b5e/9288285/b07a817cf211/OMCL2022-1296816.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b5e/9288285/4265d8e6464b/OMCL2022-1296816.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b5e/9288285/cba6c06fabaf/OMCL2022-1296816.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b5e/9288285/31a77d9157f9/OMCL2022-1296816.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b5e/9288285/c42b64048db9/OMCL2022-1296816.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b5e/9288285/b07a817cf211/OMCL2022-1296816.007.jpg

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