长链非编码RNA sox2重叠转录物的沉默通过上调miRNA-146a-5p减轻心肌缺血/再灌注损伤。

IF 1.3 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY General physiology and biophysics Pub Date : 2023-03-01 DOI:10.4149/gpb_2022065
Zhongxin Li, Guangdong Liu, Hua Huang
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引用次数: 4

摘要

长链非编码rna (lncRNAs)参与心肌缺血/再灌注损伤(MIRI)的发生发展。在本研究中,我们旨在探讨lncRNA sox2 -overlap transcript (SOX2-OT)在MIRI中的调控作用及机制。MTT法检测氧葡萄糖剥夺/再灌注(OGD/R)处理的H9c2细胞活力。ELISA法检测各组大鼠血清白细胞介素(IL)-1β、IL-6、肿瘤坏死因子(TNF)-α、丙二醛(MDA)、超氧化物歧化酶(SOD)水平。通过lnbase预测SOX2-OT和miR-146a-5p之间的靶标关系,随后通过双荧光素酶报告基因试验证实。在MIRI大鼠中进一步验证SOX2-OT沉默对心肌细胞凋亡和功能的影响。SOX2-OT在OGD/ r处理的H9c2细胞和MIRI大鼠心肌组织中表达升高。SOX2-OT的沉默提高了OGD/ r处理的H9c2细胞的活力,抑制了炎症和氧化应激。SOX2-OT负性调控其靶标miR-146a-5p。miR-146a-5p的沉默逆转了sh-SOX2-OT对OGD/ r处理的H9c2细胞的作用。此外,SOX2-OT的沉默还能减轻MIRI大鼠心肌凋亡,改善心肌功能。SOX2-OT的沉默通过上调miR-146a-5p减轻心肌细胞的凋亡、炎症和氧化应激,有助于MIRI的缓解。
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Silencing of long non-coding RNA SOX2-overlapping transcript relieves myocardial ischemia/reperfusion injury through up-regulating miRNA-146a-5p.

Long non-coding RNAs (lncRNAs) are involved in the development of myocardial ischemia/reperfusion injury (MIRI). In this study, we aimed to explore the regulatory effect and mechanism of lncRNA SOX2-overlapping transcript (SOX2-OT) in MIRI. The viability of oxygen and glucose deprivation/reperfusion (OGD/R)-treated H9c2 cells was detected by MTT assay. The levels of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, malondialdehyde (MDA), and superoxide dismutase (SOD) were measured by ELISA. The target relationship between SOX2-OT and miR-146a-5p was predicted by LncBase, and subsequently confirmed by Dual luciferase reporter assay. The effects of SOX2-OT silencing on myocardial apoptosis and function were further validated in MIRI rats. The expression of SOX2-OT was increased in OGD/R-treated H9c2 cells and myocardial tissues of MIRI rats. Silencing of SOX2-OT increased the viability and inhibited the inflammation and oxidative stress of OGD/R-treated H9c2 cells. SOX2-OT negatively regulated its target miR-146a-5p. Silencing of miR-146a-5p reversed the effects of sh-SOX2-OT on OGD/R-treated H9c2 cells. In addition, silencing of SOX2-OT also alleviated myocardial apoptosis and improved myocardial function in MIRI rats. Silencing of SOX2-OT relieved the apoptosis, inflammation, and oxidative stress of myocardial cells via up-regulating miR-146a-5p, contributing to the remission of MIRI.

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来源期刊
General physiology and biophysics
General physiology and biophysics 生物-生化与分子生物学
CiteScore
2.70
自引率
0.00%
发文量
42
审稿时长
6-12 weeks
期刊介绍: General Physiology and Biophysics is devoted to the publication of original research papers concerned with general physiology, biophysics and biochemistry at the cellular and molecular level and is published quarterly by the Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences.
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