Silencing circRUFY1 protects retinal ganglion cell injury in acute intraocular hypertension by activating the ERK pathway through miR-196a-5p/CALM3 axis

IF 1.1 4区医学 Q4 TOXICOLOGY Molecular & Cellular Toxicology Pub Date : 2024-07-02 DOI:10.1007/s13273-024-00469-z

BinBin Li, ShaoJun Li, Wei Tang, Min Zeng

{"title":"Silencing circRUFY1 protects retinal ganglion cell injury in acute intraocular hypertension by activating the ERK pathway through miR-196a-5p/CALM3 axis","authors":"BinBin Li, ShaoJun Li, Wei Tang, Min Zeng","doi":"10.1007/s13273-024-00469-z","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Neuroinflammation has been recognized as a key pathological event in acute glaucoma. Medical treatment of acute glaucoma has mainly focused on lowering intraocular pressure, yet the majority of patients still experience deterioration. Aberrant expression or activity of circular RNAs in the retina has been described in various ophthalmic diseases.</p><h3 data-test=\"abstract-sub-heading\">Objective</h3><p>This study surveyed the mechanism of circRUFY1 in acute ocular hypertension (AOH)-induced retinal ganglion cell (RGC) injury.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>AOH rats expressed high circRUFY1 and CALM3, and low miR-196a-5p in the retina tissue. CircRUFY1 silencing in AOH-induced rats reduced the severity of retinal damage and RGC damage. CircRUFY1, as a ceRNA of miR-196a-5p, upregulated CALM3, and CALM3 overexpression could further activate the ERK pathway signaling in RGCs.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>Silence of circRUFY1 protects RGCs from AOH injury mainly by inhibiting the ERK signaling pathway by regulating the miR-196a-5p/CALM3 axis. Overall, targeted intervention of circRUFY1 expression is a promising therapeutic strategy for treating RGC damage in acute glaucoma.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"11 1","pages":""},"PeriodicalIF":1.1000,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & Cellular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s13273-024-00469-z","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"TOXICOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background

Neuroinflammation has been recognized as a key pathological event in acute glaucoma. Medical treatment of acute glaucoma has mainly focused on lowering intraocular pressure, yet the majority of patients still experience deterioration. Aberrant expression or activity of circular RNAs in the retina has been described in various ophthalmic diseases.

Objective

This study surveyed the mechanism of circRUFY1 in acute ocular hypertension (AOH)-induced retinal ganglion cell (RGC) injury.

Results

AOH rats expressed high circRUFY1 and CALM3, and low miR-196a-5p in the retina tissue. CircRUFY1 silencing in AOH-induced rats reduced the severity of retinal damage and RGC damage. CircRUFY1, as a ceRNA of miR-196a-5p, upregulated CALM3, and CALM3 overexpression could further activate the ERK pathway signaling in RGCs.

Conclusion

Silence of circRUFY1 protects RGCs from AOH injury mainly by inhibiting the ERK signaling pathway by regulating the miR-196a-5p/CALM3 axis. Overall, targeted intervention of circRUFY1 expression is a promising therapeutic strategy for treating RGC damage in acute glaucoma.

Abstract Image

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

通过 miR-196a-5p/CALM3 轴激活 ERK 通路，沉默 circRUFY1 保护急性眼内高压症中的视网膜神经节细胞损伤

背景神经炎症已被认为是急性青光眼的关键病理事件。急性青光眼的药物治疗主要集中于降低眼压，但大多数患者的病情仍在恶化。本研究调查了circRUFY1在急性眼压过高（AOH）诱导的视网膜神经节细胞（RGC）损伤中的作用机制。结果AOH大鼠视网膜组织中表达高circRUFY1和CALM3，低miR-196a-5p。在 AOH 诱导的大鼠中沉默 CircRUFY1 可减轻视网膜损伤和 RGC 损伤的严重程度。结论沉默 circRUFY1 主要是通过调节 miR-196a-5p/CALM3 轴来抑制 ERK 信号通路，从而保护 RGC 免受 AOH 损伤。总之，靶向干预circRUFY1的表达是治疗急性青光眼RGC损伤的一种很有前景的治疗策略。

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分钟内获得全文去求助

来源期刊

Molecular & Cellular Toxicology 医学-毒理学

CiteScore

2.50

自引率

17.60%

发文量

114

审稿时长

6-12 weeks

期刊介绍： Molecular & Cellular Toxicology publishes original research and reviews in all areas of the complex interaction between the cell´s genome (the sum of all genes within the chromosome), chemicals in the environment, and disease. Acceptable manuscripts are the ones that deal with some topics of environmental contaminants, including those that lie in the domains of analytical chemistry, biochemistry, pharmacology and toxicology with the aspects of molecular and cellular levels. Emphasis will be placed on toxic effects observed at relevant genomics and proteomics, which have direct impact on drug development, environment health, food safety, preventive medicine, and forensic medicine. The journal is committed to rapid peer review to ensure the publication of highest quality original research and timely news and review articles.