IOCAS-IR  > 实验海洋生物学重点实验室
LncRNA pol-lnc78 as a ceRNA regulates antibacterial responses via suppression of pol-miR-n199-3p-mediated SARM down-regulation in Paralichthys olivaceus
Ning, Xian-Hui1,2; Han, Bing1; Peng, Ye1; Yin, Shao-Wu1,3
2024-01-18
发表期刊ZOOLOGICAL RESEARCH
ISSN2095-8137
卷号45期号:1页码:25-35
通讯作者Yin, Shao-Wu(yinshaowu@163.com)
摘要Long non-coding RNAs (lncRNAs) function as key modulators in mammalian immunity, particularly due to their involvement in lncRNA-mediated competitive endogenous RNA (ceRNA) crosstalk. Despite their recognized significance in mammals, research on lncRNAs in lower vertebrates remains limited. In the present study, we characterized the first immune-related lncRNA (pol-lnc78) in the teleost Japanese flounder (Paralichthys olivaceus). Results indicated that pol-lnc78 acted as a ceRNA for pol-miR-n199-3p to target the sterile alpha and armadillo motif-containing protein (SARM), the fifth discovered member of the Toll/interleukin 1 (IL-1) receptor (TIR) adaptor family. This ceRNA network regulated the antibacterial responses of flounder via the Toll-like receptor (TLR) signaling pathway. Specifically, SARM acted as a negative regulator and exacerbated bacterial infection by inhibiting the expression of inflammatory cytokines IL-1 beta and tumor necrosis factor-alpha (TNF-alpha). Pol-miR-n199-3p reduced SARM expression by specifically interacting with the 3' untranslated region (UTR), thereby promoting SARM-dependent inflammatory cytokine expression and protecting the host against bacterial dissemination. Furthermore, pol-lnc78 sponged pol-miR-n199-3p to ameliorate the inhibition of SARM expression. During infection, the negative regulators pol-lnc78 and SARM were significantly down-regulated, while pol-miR-n199-3p was significantly up-regulated, thus favoring host antibacterial defense. These findings provide novel insights into the mechanisms underlying fish immunity and open new horizons to better understand ceRNA crosstalk in lower vertebrates.
关键词LncRNA SARM miRNA ceRNA Antibacterial response
DOI10.24272/j.issn.2095-8137.2022.520
收录类别SCI
语种英语
资助项目National Natural Science Foundation of China[42006082] ; Natural Science Foundation of Jiangsu Province of China[BK20221323] ; JBGS Project of Seed Industry Revitalization in Jiangsu Province[JBGS [2021] 034] ; State Key Laboratory of Developmental Biology of Freshwater Fish[2021KF009]
WOS研究方向Zoology
WOS类目Zoology
WOS记录号WOS:001165342100002
出版者SCIENCE PRESS
WOS关键词LONG NONCODING RNA ; VIBRIO-ANGUILLARUM ; MOLECULAR CHARACTERIZATION ; CAENORHABDITIS-ELEGANS ; TRANSCRIPTOME ANALYSIS ; IMMUNE-RESPONSE ; INNATE IMMUNITY ; MESSENGER-RNA ; PROTEIN ; MIRNAS
引用统计
文献类型期刊论文
条目标识符http://ir.qdio.ac.cn/handle/337002/184602
专题实验海洋生物学重点实验室
通讯作者Yin, Shao-Wu
作者单位1.Nanjing Normal Univ, Coll Marine Sci & Engn, Nanjing 210023, Jiangsu, Peoples R China
2.Chinese Acad Sci, Inst Oceanol, Ctr Ocean Mega Sci, CAS Key Lab Expt Marine Biol, Qingdao 266071, Shandong, Peoples R China
3.Coinnovat Ctr Marine Bioind Technol Jiangsu Prov, Lianyungang 222005, Jiangsu, Peoples R China
第一作者单位中国科学院海洋研究所
推荐引用方式
GB/T 7714
Ning, Xian-Hui,Han, Bing,Peng, Ye,et al. LncRNA pol-lnc78 as a ceRNA regulates antibacterial responses via suppression of pol-miR-n199-3p-mediated SARM down-regulation in Paralichthys olivaceus[J]. ZOOLOGICAL RESEARCH,2024,45(1):25-35.
APA Ning, Xian-Hui,Han, Bing,Peng, Ye,&Yin, Shao-Wu.(2024).LncRNA pol-lnc78 as a ceRNA regulates antibacterial responses via suppression of pol-miR-n199-3p-mediated SARM down-regulation in Paralichthys olivaceus.ZOOLOGICAL RESEARCH,45(1),25-35.
MLA Ning, Xian-Hui,et al."LncRNA pol-lnc78 as a ceRNA regulates antibacterial responses via suppression of pol-miR-n199-3p-mediated SARM down-regulation in Paralichthys olivaceus".ZOOLOGICAL RESEARCH 45.1(2024):25-35.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Ning, Xian-Hui]的文章
[Han, Bing]的文章
[Peng, Ye]的文章
百度学术
百度学术中相似的文章
[Ning, Xian-Hui]的文章
[Han, Bing]的文章
[Peng, Ye]的文章
必应学术
必应学术中相似的文章
[Ning, Xian-Hui]的文章
[Han, Bing]的文章
[Peng, Ye]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。