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CONTACT General Physiology and Biophysics 2023 General Physiology and Biophysics Vol.42, No.2, p. 191–199, 2023
CONTACT General Physiology and Biophysics 2023 General Physiology and Biophysics Vol.42, No.2, p. 191–199, 2023
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General Physiology and Biophysics Vol.42, No.2, p. 191–199, 2023 |
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| Title: Silencing of long non-coding RNA SOX2-overlapping transcript relieves myocardial ischemia/reperfusion injury through up-regulating miRNA-146a-5p | ||
| Author: Zhongxin Li, Guangdong Liu, Hua Huang | ||
| Abstract: 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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| Keywords: SOX2-OT — miR-146a-5p — Myocardial ischemia/reperfusion injury — Inflammation | ||
| Published online: 14-Mar-2023 | ||
| Year: 2023, Volume: 42, Issue: 2 | Page From: 191, Page To: 199 | |
| doi:10.4149/gpb_2022065 |
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