RNA-Seq Analysis Reveals DPYSL2 and PNKD Promotes Cardiomyocytes Differentiation during Reprogramming

Yaofei Wu
{"title":"RNA-Seq Analysis Reveals DPYSL2 and PNKD Promotes Cardiomyocytes Differentiation during Reprogramming","authors":"Yaofei Wu","doi":"10.1145/3512452.3512458","DOIUrl":null,"url":null,"abstract":"Cardiomyocytes are terminally differentiated cells in the heart, whose injuries leads to severe health issue including cardiac failure and even death. Traditional medical procedure failed to rescue damaged cardiomyocytes and hence cannot cure severe myocardial damage. This is probably caused by the irreplaceability of limited cardiomyocytes number in our heart. Fortunately, recent studies reveal induced pluripotent stem cells (iPSCs) can be trained to differentiating into cardiomyocytes, opening the possibility of replacing damaged cardiomyocytes by reprogrammed iPSCs, though many remains unknow during cardiomyocytes reprogramming. In this project, we analyzed multiple RNA-Seq data during cardiomyocytes differentiation and reprogramming. We found potential candidate genes DPYSL2 and PNKD as well as several other genes that might play an important role in regulating cardiomyocytes reprogramming. We also proposed the possible mechanisms for these candidate genes based on their genetic nature as well as multi-omic data from public database. Hopefully, these studies could provide new insights on how cardiomyocytes differentiation were regulated during reprogramming and hence improving current iPSCs therapy for myocardial damage.","PeriodicalId":120446,"journal":{"name":"Proceedings of the 2021 5th International Conference on Computational Biology and Bioinformatics","volume":"162 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2021-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Proceedings of the 2021 5th International Conference on Computational Biology and Bioinformatics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1145/3512452.3512458","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

Cardiomyocytes are terminally differentiated cells in the heart, whose injuries leads to severe health issue including cardiac failure and even death. Traditional medical procedure failed to rescue damaged cardiomyocytes and hence cannot cure severe myocardial damage. This is probably caused by the irreplaceability of limited cardiomyocytes number in our heart. Fortunately, recent studies reveal induced pluripotent stem cells (iPSCs) can be trained to differentiating into cardiomyocytes, opening the possibility of replacing damaged cardiomyocytes by reprogrammed iPSCs, though many remains unknow during cardiomyocytes reprogramming. In this project, we analyzed multiple RNA-Seq data during cardiomyocytes differentiation and reprogramming. We found potential candidate genes DPYSL2 and PNKD as well as several other genes that might play an important role in regulating cardiomyocytes reprogramming. We also proposed the possible mechanisms for these candidate genes based on their genetic nature as well as multi-omic data from public database. Hopefully, these studies could provide new insights on how cardiomyocytes differentiation were regulated during reprogramming and hence improving current iPSCs therapy for myocardial damage.
RNA-Seq分析显示ddpysl2和PNKD在重编程过程中促进心肌细胞分化
心肌细胞是心脏中的终末分化细胞,其损伤可导致严重的健康问题,包括心力衰竭甚至死亡。传统的医疗程序不能挽救受损的心肌细胞,因此不能治愈严重的心肌损伤。这可能是由于我们心脏中有限的心肌细胞数量的不可替代性造成的。幸运的是,最近的研究表明,诱导多能干细胞(iPSCs)可以被训练分化成心肌细胞,从而开启了用重编程的iPSCs取代受损心肌细胞的可能性,尽管在心肌细胞重编程过程中仍有许多未知因素。在这个项目中,我们分析了心肌细胞分化和重编程过程中的多个RNA-Seq数据。我们发现潜在的候选基因DPYSL2和PNKD以及其他几个可能在调节心肌细胞重编程中发挥重要作用的基因。我们还根据候选基因的遗传性质和公共数据库的多组学数据提出了这些候选基因的可能机制。希望这些研究能够为重编程过程中如何调节心肌细胞分化提供新的见解,从而改善当前iPSCs治疗心肌损伤的方法。
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
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