Glucocorticoid Receptor Inhibits the Progression of Schistosomiasis Hepatic Fibrosis Through Inducing Circadian Clock Gene Per1.

IF 5 2区 医学 Q2 IMMUNOLOGY
Rui Tang, Tao Sun, Zhou Xing, XiaoBin Fan, PengYue Jiang, Bin Le, KaiWei Jia, YiLi Cai, XiaoJuan Bi, DongMei Zhang, RenYong Lin, Xing He
{"title":"Glucocorticoid Receptor Inhibits the Progression of Schistosomiasis Hepatic Fibrosis Through Inducing Circadian Clock Gene Per1.","authors":"Rui Tang, Tao Sun, Zhou Xing, XiaoBin Fan, PengYue Jiang, Bin Le, KaiWei Jia, YiLi Cai, XiaoJuan Bi, DongMei Zhang, RenYong Lin, Xing He","doi":"10.1093/infdis/jiaf104","DOIUrl":null,"url":null,"abstract":"<p><p>Hepatic fibrosis is the leading cause of morbidity and mortality in schistosomiasis, and transcription factors (TF) may become potential therapeutic targets for this disease. Here, we found that a TF, NR3C1, was significantly downregulated in hepatic stellate cells (HSC), the effector cell of hepatic fibrosis, from mice infected with Schistosoma japonicum using RNA sequencing. Activation of NR3C1 using dexamethasone blocked HSC activation and hepatic fibrosis progression, while these effects were completely abolished upon specific deletion of NR3C1 in HSCs. Genome-wide binding site and transcriptome analyses suggested that Per1, a circadian clock gene, was under the direct control of NR3C1 through binding the glucocorticoid response elements, and it was responsible for the inhibitory effect of NR3C1 on HSC activation. Therefore, NR3C1 is a key TF in the activation of HSCs and a potential therapeutic target for hepatic schistosomiasis.</p>","PeriodicalId":50179,"journal":{"name":"Journal of Infectious Diseases","volume":" ","pages":""},"PeriodicalIF":5.0000,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Infectious Diseases","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/infdis/jiaf104","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Hepatic fibrosis is the leading cause of morbidity and mortality in schistosomiasis, and transcription factors (TF) may become potential therapeutic targets for this disease. Here, we found that a TF, NR3C1, was significantly downregulated in hepatic stellate cells (HSC), the effector cell of hepatic fibrosis, from mice infected with Schistosoma japonicum using RNA sequencing. Activation of NR3C1 using dexamethasone blocked HSC activation and hepatic fibrosis progression, while these effects were completely abolished upon specific deletion of NR3C1 in HSCs. Genome-wide binding site and transcriptome analyses suggested that Per1, a circadian clock gene, was under the direct control of NR3C1 through binding the glucocorticoid response elements, and it was responsible for the inhibitory effect of NR3C1 on HSC activation. Therefore, NR3C1 is a key TF in the activation of HSCs and a potential therapeutic target for hepatic schistosomiasis.

求助全文
约1分钟内获得全文 求助全文
来源期刊
Journal of Infectious Diseases
Journal of Infectious Diseases 医学-传染病学
CiteScore
13.50
自引率
3.10%
发文量
449
审稿时长
2-4 weeks
期刊介绍: Published continuously since 1904, The Journal of Infectious Diseases (JID) is the premier global journal for original research on infectious diseases. The editors welcome Major Articles and Brief Reports describing research results on microbiology, immunology, epidemiology, and related disciplines, on the pathogenesis, diagnosis, and treatment of infectious diseases; on the microbes that cause them; and on disorders of host immune responses. JID is an official publication of the Infectious Diseases Society of America.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信