miR-214-3p inhibits LPS-induced macrophage inflammation and attenuates the progression of dry eye syndrome by regulating ferroptosis in cells.

IF 1.6 4区生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & genomics Pub Date : 2024-11-20 DOI:10.1007/s13258-024-01598-4

Dandan Zhao, Hao Ji, Weijia Zhang, Anni He, Caizhe Guo, Li Ma, Yan Liu

{"title":"miR-214-3p inhibits LPS-induced macrophage inflammation and attenuates the progression of dry eye syndrome by regulating ferroptosis in cells.","authors":"Dandan Zhao, Hao Ji, Weijia Zhang, Anni He, Caizhe Guo, Li Ma, Yan Liu","doi":"10.1007/s13258-024-01598-4","DOIUrl":null,"url":null,"abstract":"Background: Dry eye disease (DED) is an ocular illness caused by insufficient tear secretion or poor tear quality, and inflammation is a key factor in its pathogenesis. Previous studies have shown that miRNAs are important regulatory factors in DED.Objective: The purpose of this study was to explore the potential mechanism by which miR-214-3p influenced the DED process by regulating the macrophage inflammatory response.Methods: We induced THP-1 cells to differentiate into M0 macrophages with 100 ng/mL phorbol-12-myristate-13-acetate (PMA) and then added 15 ng/mL lipopolysaccharide (LPS) to induce inflammation. The expression of related genes and proteins was detected via RT‒qPCR, Western blotting, ELISA and immunofluorescence staining; cell viability was measured using the CCK-8 assay; and flow cytometry was used to detect ROS levels.Results: In tear and serum samples from DED patients, the levels of miR-214-3p, IL-10, and Arg1 were decreased, and the levels of IL-6, TNF-α, IL-1β, and iNOS expression were increased. Moreover, the overexpression of miR-214-3p attenuated the effect of LPS and inhibited M1 polarization and inflammation in macrophages. Mechanistically, miR-214-3p inhibited macrophage ferroptosis by downregulating TFRC expression, thereby inhibiting macrophage M1 polarization and inflammation and alleviating the progression of DED.Conclusions: Our study indicated that the upregulation of miR-214-3p expression might be a new target for DED therapy.","PeriodicalId":12675,"journal":{"name":"Genes & genomics","volume":" ","pages":""},"PeriodicalIF":1.6000,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Genes & genomics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s13258-024-01598-4","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background: Dry eye disease (DED) is an ocular illness caused by insufficient tear secretion or poor tear quality, and inflammation is a key factor in its pathogenesis. Previous studies have shown that miRNAs are important regulatory factors in DED.

Objective: The purpose of this study was to explore the potential mechanism by which miR-214-3p influenced the DED process by regulating the macrophage inflammatory response.

Methods: We induced THP-1 cells to differentiate into M0 macrophages with 100 ng/mL phorbol-12-myristate-13-acetate (PMA) and then added 15 ng/mL lipopolysaccharide (LPS) to induce inflammation. The expression of related genes and proteins was detected via RT‒qPCR, Western blotting, ELISA and immunofluorescence staining; cell viability was measured using the CCK-8 assay; and flow cytometry was used to detect ROS levels.

Results: In tear and serum samples from DED patients, the levels of miR-214-3p, IL-10, and Arg1 were decreased, and the levels of IL-6, TNF-α, IL-1β, and iNOS expression were increased. Moreover, the overexpression of miR-214-3p attenuated the effect of LPS and inhibited M1 polarization and inflammation in macrophages. Mechanistically, miR-214-3p inhibited macrophage ferroptosis by downregulating TFRC expression, thereby inhibiting macrophage M1 polarization and inflammation and alleviating the progression of DED.

Conclusions: Our study indicated that the upregulation of miR-214-3p expression might be a new target for DED therapy.

查看原文本刊更多论文

miR-214-3p 通过调节细胞中的铁蛋白沉积抑制 LPS 诱导的巨噬细胞炎症并减轻干眼症的进展。

背景：干眼症（DED）是一种由泪液分泌不足或泪液质量差引起的眼部疾病，炎症是其发病机制中的一个关键因素。以往的研究表明，miRNA 是 DED 的重要调控因子：本研究旨在探讨 miR-214-3p 通过调节巨噬细胞炎症反应影响 DED 过程的潜在机制：方法：我们用 100 ng/mL 磷脂醇-12-肉豆蔻酸-13-乙酸酯（PMA）诱导 THP-1 细胞分化成 M0 巨噬细胞，然后加入 15 ng/mL 脂多糖（LPS）诱导炎症反应。通过RT-qPCR、Western印迹、ELISA和免疫荧光染色检测相关基因和蛋白质的表达；使用CCK-8测定法测量细胞活力；使用流式细胞术检测ROS水平：结果：在 DED 患者的泪液和血清样本中，miR-214-3p、IL-10 和 Arg1 水平下降，IL-6、TNF-α、IL-1β 和 iNOS 表达水平升高。此外，过表达 miR-214-3p 可减轻 LPS 的作用，抑制巨噬细胞的 M1 极化和炎症反应。从机理上讲，miR-214-3p 通过下调 TFRC 的表达抑制巨噬细胞的铁凋亡，从而抑制巨噬细胞的 M1 极化和炎症，缓解 DED 的进展：我们的研究表明，miR-214-3p表达的上调可能是DED治疗的一个新靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Genes & genomics 生物-生化与分子生物学

CiteScore

3.70

自引率

4.80%

发文量

131

审稿时长

6-12 weeks

期刊介绍： Genes & Genomics is an official journal of the Korean Genetics Society (http://kgenetics.or.kr/). Although it is an official publication of the Genetics Society of Korea, membership of the Society is not required for contributors. It is a peer-reviewed international journal publishing print (ISSN 1976-9571) and online version (E-ISSN 2092-9293). It covers all disciplines of genetics and genomics from prokaryotes to eukaryotes from fundamental heredity to molecular aspects. The articles can be reviews, research articles, and short communications.