MiR-922 alleviates LPS-induced HK-2 cell apoptosis and inflammation through TGF-β/Smad.

IF 1.1 4区生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY

Nucleosides, Nucleotides & Nucleic Acids Pub Date : 2025-06-22 DOI:10.1080/15257770.2025.2518554

Bo Yang, Li Xu, Peng Zhou, Qihao Ma, Yong Li, Danan Sun

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引用次数: 0

Abstract

Background: MicroRNAs play an extensive role in human chronic kidney diseases (CKD), but the role of miR-922 remains unclear.

Purpose: This study was designed to investigate the potential mechanism by which miR-922 acts in CKD.

Methods: The human proximal renal tubular cell line (HK-2) was treated by LPS to build a CKD cell model. The expressions of miR-922, TGFβR1, and p-Smad2/3 were detected by RT-qPCR or western blotting. The dual-luciferase reporter assay verified the interaction of miR-922 with TGFβR1. Cell viability and apoptosis were assessed using the CCK-8 assay and Annexin V-FITC/PI method. An ELISA kit was used for the measure of TNF-α/IL-1β levels.

Results: MiR-922 was scanty in HK-2 cells with LPS treatment. MiR-922 was an upstream regulator of TGFβR1. The up-regulation of miR-922 restrained TGFβR1 expression, thereby hindering the activation of Smad2/3. Overexpression of miR-922 and inhibition of Smad2/3 alleviated the LPS-induced apoptosis and inflammation, while TGFβR1 played a pro-apoptotic and pro-inflammatory role.

Conclusion: MiR-922 rescued HK-2 cell apoptosis and inflammation damage induced by LPS through negative regulation of TGF-β/Smad pathway, which may be a vital molecular mechanism of CKD.

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MiR-922通过TGF-β/Smad缓解lps诱导的HK-2细胞凋亡和炎症。

背景：microrna在人类慢性肾脏疾病（CKD）中发挥着广泛的作用，但miR-922的作用尚不清楚。目的：本研究旨在探讨miR-922在CKD中作用的潜在机制。方法：采用LPS处理人肾近端小管细胞系HK-2，建立CKD细胞模型。RT-qPCR或western blotting检测miR-922、TGFβR1、p-Smad2/3的表达。双荧光素酶报告试验证实了miR-922与tgf - β r1的相互作用。采用CCK-8法和Annexin V-FITC/PI法检测细胞活力和凋亡情况。ELISA检测TNF-α/IL-1β水平。结果：LPS处理HK-2细胞中MiR-922缺失。MiR-922是tgf - β r1的上游调节因子。miR-922的上调抑制了tgf - β r1的表达，从而阻碍Smad2/3的激活。过表达miR-922和抑制Smad2/3可减轻lps诱导的细胞凋亡和炎症，tgf - β r1发挥促凋亡和促炎症作用。结论：MiR-922通过负调控TGF-β/Smad通路挽救LPS诱导的HK-2细胞凋亡和炎症损伤，这可能是CKD的重要分子机制。

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

Nucleosides, Nucleotides & Nucleic Acids 生物-生化与分子生物学

CiteScore

2.60

自引率

7.70%

发文量

审稿时长

6 months

期刊介绍： Nucleosides, Nucleotides & Nucleic Acids publishes research articles, short notices, and concise, critical reviews of related topics that focus on the chemistry and biology of nucleosides, nucleotides, and nucleic acids. Complete with experimental details, this all-inclusive journal emphasizes the synthesis, biological activities, new and improved synthetic methods, and significant observations related to new compounds.