Knockdown of lncRNA SNHG16 attenuates myocardial ischemia‑reoxygenation injury via targeting miR‑183/FOXO1 axis

Geng,Tao; Xu,Zesheng; Xing,Jingxian; Yuan,Yonggang; Liu,Juan

doi:10.3892/etm.2023.11805

Knockdown of lncRNA SNHG16 attenuates myocardial ischemia‑reoxygenation injury via targeting miR‑183/FOXO1 axis

Authors:
- Tao Geng
- Zesheng Xu
- Jingxian Xing
- Yonggang Yuan
- Juan Liu
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Affiliations: Department of Cardiovascular Medicine, Cangzhou Central Hospital, Cangzhou, Hebei 061000, P.R. China
Published online on: January 23, 2023 https://doi.org/10.3892/etm.2023.11805
Article Number: 106
Copyright: © Geng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Accumulating evidence shows that long non‑coding RNAs (lncRNAs) are widely involved in cellular processes of myocardial ischemia/reperfusion (I/R). The present study investigated the functions of lncRNA SNHG16 in myocardial I/R and the mechanism mediated by SNHG16. The myocardial I/R rat and cell model and hypoxia/reoxygenation injury (H/R) models of H9C2 cardiomyocytes were established to detect the expression of SNHG16. Cell Counting Kit‑8, flow cytometric and western blot assays were conducted to detect cell viability, apoptosis and protein expression. Myocardial cell apoptosis was assessed by TUNEL staining. Dual‑luciferase gene reporter was applied to determine the interaction between the molecules. The expressions of SNHG16 were upregulated in myocardial I/R injury models. Inhibition of SNHG16 relieved myocardial I/R injury in vivo and in vitro silencing of SNHG16 alleviated H/R induced cardiomyocyte apoptosis. To explore the regulatory mechanism, it was discovered that SNHG16 directly interacted with miR‑183, while forkhead box O1 (FoxO1) was a target of microRNA (miR)‑183. Findings from rescue assays revealed that miR‑183 inhibitor and upregulation of FOXO1 can rescue the effect of sh‑SNHG16 on H/R‑induced cardiomyocyte apoptosis. The results indicated that the lncRNA SNHG16/miR‑183/FOXO1 axis exacerbated myocardial cell apoptosis in myocardial I/R injury, suggesting SNHG16 as a potential therapeutic target for myocardial I/R injury.

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