MicroRNA-216a-5p Alleviates Acute Kidney Injury of Mice via Suppressing FAS Ligand Expression.

IF 16.4 1区化学 Q1 CHEMISTRY, MULTIDISCIPLINARY

Accounts of Chemical Research Pub Date : 2024-01-01 Epub Date: 2024-08-02 DOI:10.1159/000539980

Biying Zhou, Ruirui Luo, Yanlin Sun, Aixiang Yang

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引用次数: 0

Abstract

Introduction: The aim of this present work was to investigate the mechanism of the microRNA (miR)-216a-5p/FASL axis in mice with acute kidney injury (AKI).

Methods: Mice kidney ischemia/reperfusion (I/R) injury was used as AKI models in this study. I/R mice were injected with miR-216a-5p- and FASL-related constructs to investigate potential mechanisms of kidney protection. Kidney function, inflammation, oxidative stress, and kidney cell apoptosis were assessed after 24 h of reperfusion. In vitro, the hypoxia-reoxygenation (H/R) model was used with kidney tubular epithelial cells (TECs) to mimic kidney I/R injury. H/R-treated TECs were transfected with miR-216a-5p- and FASL-related constructs to detect cell viability, inflammation, and oxidative stress. MiR-216a-5p and FASL expression levels in mouse kidney tissues and in H/R-treated TECs were detected.

Results: MiR-216a-5p was downregulated and FASL was upregulated in kidney tissues of I/R mice and H/R-treated TECs. Upregulating miR-216a-5p attenuated kidney cell apoptosis and the damage of kidney function, and reduced inflammatory factor levels and oxidative stress response in kidney tissues of I/R mice. Upregulating miR-216a-5p advanced cell viability and reduced inflammatory factor levels and oxidative stress response in H/R-treated TECs. Downregulation of FASL effectively reversed the influences of downregulation of miR-216a-5p on kidney injury in mice and kidney TEC survival.

Conclusion: Our study reveals that miR-216a-5p reduces I/R-induced pathological kidney damage in AKI via suppressing FASL.

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microRNA-216a-5p 通过抑制 FASL 的表达减轻小鼠急性肾损伤。

引言本研究旨在探讨急性肾损伤（AKI）小鼠体内microRNA（miR）-216a-5p/FASL轴的作用机制：方法：本研究以小鼠肾脏缺血再灌注（I/R）损伤为 AKI 模型。再灌注 24 小时后评估肾功能、炎症、氧化应激和肾细胞凋亡。在体外，利用肾小管上皮细胞（TECs）的低氧-复氧（H/R）模型模拟肾脏I/R损伤。结果：在I/R小鼠肾组织和H/R处理的TECs中，miR-216a-5p下调，FASL上调。上调 miR-216a-5p 可减轻 I/R 小鼠肾脏组织中肾细胞凋亡和肾功能损伤，降低炎症因子水平和氧化应激反应。上调miR-216a-5p可提高H/R处理的TECs细胞活力，降低炎症因子水平和氧化应激反应。下调FASL可有效逆转下调miR-216a-5p对小鼠肾损伤和肾脏TEC存活的影响：我们的研究发现，miR-216a-5p可通过抑制FASL减轻I/R诱导的AKI病理肾损伤。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Accounts of Chemical Research 化学-化学综合

CiteScore

31.40

自引率

1.10%

发文量

312

审稿时长

2 months

期刊介绍： Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance. Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.