发布求助

文献互助智能选刊最新文献

肠病毒71结构病毒蛋白1通过m6A修饰促进小鼠雪旺细胞PMP22的表达。

IF 2.7 4区医学 Q3 VIROLOGY

Virus research Pub Date : 2025-06-04 DOI:10.1016/j.virusres.2025.199590

Qiuyan Peng , Guangming Liu , Danping Zhu , Suyun Li , Sida Yang , Peiqing Li , Yingxian Yin , Dandan Hu

{"title":"肠病毒71结构病毒蛋白1通过m6A修饰促进小鼠雪旺细胞PMP22的表达。","authors":"Qiuyan Peng , Guangming Liu , Danping Zhu , Suyun Li , Sida Yang , Peiqing Li , Yingxian Yin , Dandan Hu","doi":"10.1016/j.virusres.2025.199590","DOIUrl":null,"url":null,"abstract":"<div><h3>Purpose</h3><div>Enterovirus 71 (EV71) is one of the enteroviruses that causes hand-foot-and-mouth disease (HFMD). This study aims to investigate the role of EV71 structural viral protein 1 (VP1) in mouse Schwann cells.</div></div><div><h3>Methods</h3><div>An EV71 VP1-expressing vector was generated and transfected into mouse Schwann cells (MSCs). Small interfering RNAs against methyltransferase-like protein 14 (METTL14) and YTH N<sup>6</sup>-Methyladenosine RNA Binding Protein 1 (YTHDF1) were used to knock down the expressions of METTL14 and YTHDF1 in MSCs to investigate their roles in peripheral myelin protein 22 (PMP22) expression. Real-time PCR and Western blot analysis were performed to determine the expressions of PMP22 and m<sup>6</sup>A modification-associated proteins.</div></div><div><h3>Results</h3><div>EV71-VP1 over-expression significantly increased the expressions of transmethylase METTL3/14 and m<sup>6</sup>A methylation recognition protein YTHDC1 and YTHDF1/2/3 in MSCs. On the contrary, the level of demethylase FTO, but not ALKBH5, was obviously decreased in VP1-over-expressed MSCs. Furthermore, 3-DZA inhibited expressions of METTL3/14 and YTHDF1/2 in VP1-over-expressed MSCs, indicating METTL3/14 and YTHDF1/2 were the key m<sup>6</sup>A-modification-related genes regulated by VP1. In addition, deficiency of METTL14 or YTHDF1 contracted the up-regulation of PMP22 induced by VP1 overexpression in MSCs.</div></div><div><h3>Conclusions</h3><div>VP1 up-regulated PMP22 via m6A modification in MSCs, which were mainly affected by METTL14 and YTHDF1.</div></div>","PeriodicalId":23483,"journal":{"name":"Virus research","volume":"358 ","pages":"Article 199590"},"PeriodicalIF":2.7000,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Enterovirus 71 structural viral protein 1 promotes the expression of PMP22 through m6A modification in mouse Schwann cells\",\"authors\":\"Qiuyan Peng , Guangming Liu , Danping Zhu , Suyun Li , Sida Yang , Peiqing Li , Yingxian Yin , Dandan Hu\",\"doi\":\"10.1016/j.virusres.2025.199590\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Purpose</h3><div>Enterovirus 71 (EV71) is one of the enteroviruses that causes hand-foot-and-mouth disease (HFMD). This study aims to investigate the role of EV71 structural viral protein 1 (VP1) in mouse Schwann cells.</div></div><div><h3>Methods</h3><div>An EV71 VP1-expressing vector was generated and transfected into mouse Schwann cells (MSCs). Small interfering RNAs against methyltransferase-like protein 14 (METTL14) and YTH N<sup>6</sup>-Methyladenosine RNA Binding Protein 1 (YTHDF1) were used to knock down the expressions of METTL14 and YTHDF1 in MSCs to investigate their roles in peripheral myelin protein 22 (PMP22) expression. Real-time PCR and Western blot analysis were performed to determine the expressions of PMP22 and m<sup>6</sup>A modification-associated proteins.</div></div><div><h3>Results</h3><div>EV71-VP1 over-expression significantly increased the expressions of transmethylase METTL3/14 and m<sup>6</sup>A methylation recognition protein YTHDC1 and YTHDF1/2/3 in MSCs. On the contrary, the level of demethylase FTO, but not ALKBH5, was obviously decreased in VP1-over-expressed MSCs. Furthermore, 3-DZA inhibited expressions of METTL3/14 and YTHDF1/2 in VP1-over-expressed MSCs, indicating METTL3/14 and YTHDF1/2 were the key m<sup>6</sup>A-modification-related genes regulated by VP1. In addition, deficiency of METTL14 or YTHDF1 contracted the up-regulation of PMP22 induced by VP1 overexpression in MSCs.</div></div><div><h3>Conclusions</h3><div>VP1 up-regulated PMP22 via m6A modification in MSCs, which were mainly affected by METTL14 and YTHDF1.</div></div>\",\"PeriodicalId\":23483,\"journal\":{\"name\":\"Virus research\",\"volume\":\"358 \",\"pages\":\"Article 199590\"},\"PeriodicalIF\":2.7000,\"publicationDate\":\"2025-06-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Virus research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S016817022500067X\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"VIROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Virus research","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S016817022500067X","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"VIROLOGY","Score":null,"Total":0}

引用次数: 0

摘要

目的：肠病毒71 （EV71）是引起手足口病（手足口病）的肠道病毒之一。本研究旨在探讨EV71结构病毒蛋白1 （VP1）在小鼠雪旺细胞中的作用。方法：制备EV71表达载体，转染小鼠雪旺细胞（MSCs）。利用靶向甲基转移酶样蛋白14 （METTL14）和YTH n6 -甲基腺苷RNA结合蛋白1 （YTHDF1）的小干扰RNA敲低MSCs中METTL14和YTHDF1的表达，研究其在外周血髓磷脂蛋白22 （PMP22）表达中的作用。采用Real-time PCR和Western blot检测PMP22和m6A修饰相关蛋白的表达。结果：EV71-VP1过表达显著增加MSCs中转甲基化酶METTL3/14和m6A甲基化识别蛋白YTHDC1和YTHDF1/2/3的表达。相反，在vp1过表达的MSCs中，去甲基化酶FTO水平明显降低，而ALKBH5水平不明显降低。此外，3-DZA抑制过表达VP1的MSCs中METTL3/14和YTHDF1/2的表达，说明METTL3/14和YTHDF1/2是VP1调控m6a修饰的关键基因。此外，METTL14或YTHDF1的缺失使MSCs中VP1过表达诱导的PMP22上调。结论：VP1在MSCs中通过m6A修饰上调PMP22，主要受METTL14和YTHDF1的影响。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

Enterovirus 71 structural viral protein 1 promotes the expression of PMP22 through m6A modification in mouse Schwann cells

Purpose

Enterovirus 71 (EV71) is one of the enteroviruses that causes hand-foot-and-mouth disease (HFMD). This study aims to investigate the role of EV71 structural viral protein 1 (VP1) in mouse Schwann cells.

Methods

An EV71 VP1-expressing vector was generated and transfected into mouse Schwann cells (MSCs). Small interfering RNAs against methyltransferase-like protein 14 (METTL14) and YTH N⁶-Methyladenosine RNA Binding Protein 1 (YTHDF1) were used to knock down the expressions of METTL14 and YTHDF1 in MSCs to investigate their roles in peripheral myelin protein 22 (PMP22) expression. Real-time PCR and Western blot analysis were performed to determine the expressions of PMP22 and m⁶A modification-associated proteins.

Results

EV71-VP1 over-expression significantly increased the expressions of transmethylase METTL3/14 and m⁶A methylation recognition protein YTHDC1 and YTHDF1/2/3 in MSCs. On the contrary, the level of demethylase FTO, but not ALKBH5, was obviously decreased in VP1-over-expressed MSCs. Furthermore, 3-DZA inhibited expressions of METTL3/14 and YTHDF1/2 in VP1-over-expressed MSCs, indicating METTL3/14 and YTHDF1/2 were the key m⁶A-modification-related genes regulated by VP1. In addition, deficiency of METTL14 or YTHDF1 contracted the up-regulation of PMP22 induced by VP1 overexpression in MSCs.

Conclusions

VP1 up-regulated PMP22 via m6A modification in MSCs, which were mainly affected by METTL14 and YTHDF1.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

来源期刊

Virus research

Virus research 医学-病毒学

CiteScore

9.50

自引率

2.00%

发文量

239

审稿时长

43 days

期刊介绍： Virus Research provides a means of fast publication for original papers on fundamental research in virology. Contributions on new developments concerning virus structure, replication, pathogenesis and evolution are encouraged. These include reports describing virus morphology, the function and antigenic analysis of virus structural components, virus genome structure and expression, analysis on virus replication processes, virus evolution in connection with antiviral interventions, effects of viruses on their host cells, particularly on the immune system, and the pathogenesis of virus infections, including oncogene activation and transduction.

联系我们：info@booksci.cn Book学术提供免费学术资源搜索服务，方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1

京公网安备 11010802042870号

Book学术文献互助

Book学术文献互助群
群号：604180095

Book学术官方微信