miR-129-5p Induces Cell Apoptosis and Inhibits Inflammation by Inflammatory Signaling to Alleviate Spinal Cord Injury (SCI)

IF 0.1 4区 医学
Zhe-Ming Song, Yuwei Gao, Yuhao Zhao, Xiaofei Feng, Zhenjie Zhao, Wenji Wang
{"title":"miR-129-5p Induces Cell Apoptosis and Inhibits Inflammation by Inflammatory Signaling to Alleviate Spinal Cord Injury (SCI)","authors":"Zhe-Ming Song, Yuwei Gao, Yuhao Zhao, Xiaofei Feng, Zhenjie Zhao, Wenji Wang","doi":"10.1166/jbt.2023.3197","DOIUrl":null,"url":null,"abstract":"Spinal cord injury (SCI) is a spinal cord nerve dysfunction secondary to trauma. Until now, still no appropriate drug with unclear etiology. Therefore, it is to develop effective SCI treatment methods. Herein, we intended to detect the impact of miR-129-5p in SCI After establishment\n of a mouse SCI model, the animals received intrathecal injection of agomir-miR-129-5p or normal saline. Then, the miR-129-5p’s effect was evaluated by assessing motor function, spinal cord tissue edema, apoptosis and inflammation of mice upon treatments and potential targeted pathways\n of the miRNA were detected. Overexpressed miR-129-5p facilitated the wound healing with less spare tissue and water content. Additionally, overexpressed miR-129-5p suppressed the in vivo inflammation with decreased apoptotic rate of neurons. As SCI induced increased expression of HMGB1,\n TLR4, and NF-κB in tissues, but the presence of miR-129-5p reversed the expressions. Collectively, this study elucidate miR-129-5p significantly improves inflammatory response and apoptosis, thereby improving the condition of SCI. These findings might provide a new theory for\n the disorder, and promote the research progress on the disease.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":"352 5","pages":""},"PeriodicalIF":0.1000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biomaterials and Tissue Engineering","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1166/jbt.2023.3197","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Spinal cord injury (SCI) is a spinal cord nerve dysfunction secondary to trauma. Until now, still no appropriate drug with unclear etiology. Therefore, it is to develop effective SCI treatment methods. Herein, we intended to detect the impact of miR-129-5p in SCI After establishment of a mouse SCI model, the animals received intrathecal injection of agomir-miR-129-5p or normal saline. Then, the miR-129-5p’s effect was evaluated by assessing motor function, spinal cord tissue edema, apoptosis and inflammation of mice upon treatments and potential targeted pathways of the miRNA were detected. Overexpressed miR-129-5p facilitated the wound healing with less spare tissue and water content. Additionally, overexpressed miR-129-5p suppressed the in vivo inflammation with decreased apoptotic rate of neurons. As SCI induced increased expression of HMGB1, TLR4, and NF-κB in tissues, but the presence of miR-129-5p reversed the expressions. Collectively, this study elucidate miR-129-5p significantly improves inflammatory response and apoptosis, thereby improving the condition of SCI. These findings might provide a new theory for the disorder, and promote the research progress on the disease.
miR-129-5p诱导细胞凋亡并通过炎症信号抑制炎症以减轻脊髓损伤(SCI)
脊髓损伤(SCI)是一种继发于创伤的脊髓神经功能障碍。至今仍无病因不明的合适药物。因此,开发有效的脊髓损伤治疗方法势在必行。在此,我们打算检测miR-129-5p对脊髓损伤的影响。在小鼠脊髓损伤模型建立后,动物接受鞘内注射agomir-miR-129-5p或生理盐水。然后,通过评估治疗后小鼠的运动功能、脊髓组织水肿、细胞凋亡和炎症来评估miR-129-5p的作用,并检测miRNA的潜在靶向途径。过表达miR-129-5p促进创面愈合,备用组织和水分含量减少。此外,过表达的miR-129-5p抑制了体内炎症,降低了神经元的凋亡率。SCI诱导HMGB1、TLR4、NF-κB在组织中的表达增加,而miR-129-5p的存在逆转了这些表达。综上所述,本研究阐明miR-129-5p可显著改善炎症反应和细胞凋亡,从而改善脊髓损伤的病情。这些发现可能为该疾病提供一种新的理论,并促进对该疾病的研究进展。
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 求助全文
来源期刊
自引率
0.00%
发文量
332
审稿时长
>12 weeks
×
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