The changes in the ratio of Dicer1 transcripts can participate in the neuronal hypoxic response by regulating miR-29b.

IF 2.9 2区 医学 Q2 NEUROSCIENCES Cerebral cortex Pub Date : 2025-02-05 DOI:10.1093/cercor/bhae490
Linan Liu, Yingxin Liu, Yongfeng Sun, Xian Lu, Yong Ji, Xiujuan Zhao, Jun Li, Chuncheng Liu
{"title":"The changes in the ratio of Dicer1 transcripts can participate in the neuronal hypoxic response by regulating miR-29b.","authors":"Linan Liu, Yingxin Liu, Yongfeng Sun, Xian Lu, Yong Ji, Xiujuan Zhao, Jun Li, Chuncheng Liu","doi":"10.1093/cercor/bhae490","DOIUrl":null,"url":null,"abstract":"<p><p>The nervous system is highly dependent on the supply of oxygen and nutrients, so when demand for oxygen exceeds its supply, hypoxia is induced. The hippocampus is very important in the nervous system. It has the ability to control human behavior, memory, emotion, and so on. Therefore, when the hippocampus is damaged by hypoxia, it may cause nervous system diseases such as Alzheimer's disease, Parkinson's disease, and stroke. Alternative splicing plays an important regulatory role in the processes of growth and disease occurrence and development. However, the function of hypoxia-induced alternative splicing in neurological diseases needs to be further studied. Therefore, we performed hypoxia stress on mouse hippocampal neuron HT22 cells and then analyzed differentially expressed genes and differential alternative splicing events by next-generation sequencing. Through bioinformatics analysis and verification, it was found that hypoxia stress regulated the expression of Rbm15 and the ratio of Dicer1 transcripts in HT22 cells. The change in the ratio of Dicer1 transcripts may be related to the upregulation of miR-29b under hypoxia stress. This study can provide multiple time point sequencing results and a theoretical basis for the study of hypoxia-related gene alternative splicing.</p>","PeriodicalId":9715,"journal":{"name":"Cerebral cortex","volume":" ","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cerebral cortex","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/cercor/bhae490","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

The nervous system is highly dependent on the supply of oxygen and nutrients, so when demand for oxygen exceeds its supply, hypoxia is induced. The hippocampus is very important in the nervous system. It has the ability to control human behavior, memory, emotion, and so on. Therefore, when the hippocampus is damaged by hypoxia, it may cause nervous system diseases such as Alzheimer's disease, Parkinson's disease, and stroke. Alternative splicing plays an important regulatory role in the processes of growth and disease occurrence and development. However, the function of hypoxia-induced alternative splicing in neurological diseases needs to be further studied. Therefore, we performed hypoxia stress on mouse hippocampal neuron HT22 cells and then analyzed differentially expressed genes and differential alternative splicing events by next-generation sequencing. Through bioinformatics analysis and verification, it was found that hypoxia stress regulated the expression of Rbm15 and the ratio of Dicer1 transcripts in HT22 cells. The change in the ratio of Dicer1 transcripts may be related to the upregulation of miR-29b under hypoxia stress. This study can provide multiple time point sequencing results and a theoretical basis for the study of hypoxia-related gene alternative splicing.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Dicer1转录本比例的变化可以通过调节miR-29b参与神经元缺氧反应。
神经系统高度依赖氧气和营养物质的供应,因此当氧气的需求超过其供应时,就会引起缺氧。海马体在神经系统中非常重要。它有能力控制人类的行为、记忆、情感等等。因此,当海马因缺氧而受损时,可能会引起阿尔茨海默病、帕金森病、中风等神经系统疾病。选择性剪接在植物生长和疾病发生发展过程中起着重要的调控作用。然而,缺氧诱导的选择性剪接在神经系统疾病中的作用有待进一步研究。因此,我们对小鼠海马神经元HT22细胞进行缺氧应激,然后通过下一代测序分析差异表达基因和差异选择性剪接事件。通过生物信息学分析和验证,发现缺氧胁迫可调节HT22细胞中Rbm15的表达和Dicer1转录本的比例。Dicer1转录本比例的变化可能与缺氧胁迫下miR-29b的上调有关。本研究可为缺氧相关基因选择性剪接的研究提供多时间点测序结果和理论基础。
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
Cerebral cortex
Cerebral cortex 医学-神经科学
CiteScore
6.30
自引率
8.10%
发文量
510
审稿时长
2 months
期刊介绍: Cerebral Cortex publishes papers on the development, organization, plasticity, and function of the cerebral cortex, including the hippocampus. Studies with clear relevance to the cerebral cortex, such as the thalamocortical relationship or cortico-subcortical interactions, are also included. The journal is multidisciplinary and covers the large variety of modern neurobiological and neuropsychological techniques, including anatomy, biochemistry, molecular neurobiology, electrophysiology, behavior, artificial intelligence, and theoretical modeling. In addition to research articles, special features such as brief reviews, book reviews, and commentaries are included.
期刊最新文献
Aging-related losses in dopamine D2/3 receptor availability are linked to working-memory decline across five years. Diagnosis of Alzheimer's disease using FusionNet with improved secretary bird optimization algorithm for optimal MK-SVM based on imaging genetic data. Differential neurogenic patterns underlie the formation of primary and secondary areas in the developing somatosensory cortex. Identifying causal neural oscillations underlying working memory. Neural correlates of reciprocity bias: social debts modulate unfairness perception of violation during third-party observation.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1