Downregulating EVA1C exerts the potential to promote neuron growth after neonatal hypoxic-ischemic encephalopathy injury associated with alternative splicing

Ibrain Pub Date : 2022-07-21 DOI:10.1002/ibra.12053
Yue Hu, Rong Rong, Yi Wang, Shan-Shan Yan, Su Liu, Lei Wang
{"title":"Downregulating EVA1C exerts the potential to promote neuron growth after neonatal hypoxic-ischemic encephalopathy injury associated with alternative splicing","authors":"Yue Hu,&nbsp;Rong Rong,&nbsp;Yi Wang,&nbsp;Shan-Shan Yan,&nbsp;Su Liu,&nbsp;Lei Wang","doi":"10.1002/ibra.12053","DOIUrl":null,"url":null,"abstract":"<p>Neonatal hypoxic-ischemic encephalopathy (NHIE) is one of the major diseases in newborns during the perinatal stage, which globally is the main reason for children's morbidity and mortality. However, the mechanism of NHIE still remains poorly clear. In this study, the 7-day-old rats were subjected to hypoxic-ischemia (HI), then brain damage was detected. Afterward, the expression of eva-1 homolog C (EVA1C) was measured in vitro by establishing the oxygen-glucose deprivation (OGD) model in SHSY5Y cells and human fetal neurons. Subsequently, the potential function and mechanism of EVA1C were explored by silencing EVA1C and alternative splicing prediction. As a result, obvious neurobehavioral impairment and brain infarction were detected through Zea-Longa score and TTC staining; meanwhile, neuron injury was tested by HE and Nissl staining post HI. Moreover, it was found that the expression of EVA1C was notably upregulated in SHSY5Y cells and human fetal neurons after OGD. In addition, cell survival and growth were increased after silencing EVA1C, which might be associated with alternative splicing. In conclusion, EVA1C interference exhibited potential in promoting neuron survival and growth, associated with exon skipping with the alternative splicing site in 34613318:34687258, which may provide the basis for the therapeutic target and mechanism research of NHIE.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":"8 4","pages":"481-491"},"PeriodicalIF":0.0000,"publicationDate":"2022-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10529346/pdf/IBRA-8-481.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Ibrain","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/ibra.12053","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Neonatal hypoxic-ischemic encephalopathy (NHIE) is one of the major diseases in newborns during the perinatal stage, which globally is the main reason for children's morbidity and mortality. However, the mechanism of NHIE still remains poorly clear. In this study, the 7-day-old rats were subjected to hypoxic-ischemia (HI), then brain damage was detected. Afterward, the expression of eva-1 homolog C (EVA1C) was measured in vitro by establishing the oxygen-glucose deprivation (OGD) model in SHSY5Y cells and human fetal neurons. Subsequently, the potential function and mechanism of EVA1C were explored by silencing EVA1C and alternative splicing prediction. As a result, obvious neurobehavioral impairment and brain infarction were detected through Zea-Longa score and TTC staining; meanwhile, neuron injury was tested by HE and Nissl staining post HI. Moreover, it was found that the expression of EVA1C was notably upregulated in SHSY5Y cells and human fetal neurons after OGD. In addition, cell survival and growth were increased after silencing EVA1C, which might be associated with alternative splicing. In conclusion, EVA1C interference exhibited potential in promoting neuron survival and growth, associated with exon skipping with the alternative splicing site in 34613318:34687258, which may provide the basis for the therapeutic target and mechanism research of NHIE.

Abstract Image

下调EVA1C有可能促进新生儿缺氧缺血性脑病损伤后神经元的生长,并伴有选择性剪接
新生儿缺氧缺血性脑病(NHIE)是围生期新生儿的主要疾病之一,是全球儿童发病和死亡的主要原因。然而,NHIE的发病机制仍不清楚。本实验采用7日龄大鼠缺氧缺血(HI),观察脑损伤。随后,通过建立氧-葡萄糖剥夺(OGD)模型,在SHSY5Y细胞和人胎儿神经元中体外检测eva-1同源物C (EVA1C)的表达。随后,我们通过沉默EVA1C和选择性剪接预测来探索EVA1C的潜在功能和机制。结果,Zea-Longa评分、TTC染色均可见明显的神经行为障碍及脑梗死;同时,HI后用HE和尼氏染色检测神经元损伤。此外,研究发现,OGD后SHSY5Y细胞和人胎儿神经元中EVA1C的表达明显上调。此外,沉默EVA1C后细胞存活和生长增加,这可能与选择性剪接有关。综上所述,EVA1C干扰具有促进神经元存活和生长的潜力,与34613318:34687258的备选剪接位点外显子跳变有关,可为NHIE的治疗靶点和机制研究提供依据。
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
CiteScore
0.90
自引率
0.00%
发文量
0
×
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