题名 | MiR-301a promotes embryonic stem cell differentiation to cardiomyocytes |
作者 | |
发表日期 | 2019-12-26 |
发表期刊 | WORLD JOURNAL OF STEM CELLS 影响因子和分区 |
语种 | 英语 |
原始文献类型 | Article |
关键词 | miR-301a Mouse embryonic stem cells Differentiation Cardiomyocytes |
其他关键词 | PROLIFERATION ; EXPRESSION ; PROGENITORS |
摘要 | BACKGROUND Cardiovascular disease is the leading cause of death worldwide. Tissue repair after pathological injury in the heart remains a major challenge due to the limited regenerative ability of cardiomyocytes in adults. Stem cell-derived cardiomyocytes provide a promising source for the cell transplantation-based treatment of injured hearts. AIM To explore the function and mechanisms of miR-301a in regulating cardiomyocyte differentiation of mouse embryonic stem (mES) cells, and provide experimental evidence for applying miR-301a to the cardiomyocyte differentiation induction from stem cells. METHODS mES cells with or without overexpression of miR-301a were applied for all functional assays. The hanging drop technique was applied to form embryoid bodies from mES cells. Cardiac markers including GATA-4, TBX5, MEF2C, and alpha-actinin were used to determine cardiomyocyte differentiation from mES cells. RESULTS High expression of miR-301a was detected in the heart from late embryonic to neonatal mice. Overexpression of miR-301a in mES cells significantly induced the expression of cardiac transcription factors, thereby promoting cardiomyocyte differentiation and beating cardiomyocyte clone formation. PTEN is a target gene of miR-301a in cardiomyocytes. PTEN-regulated PI3K-AKT-mTOR-Stat3 signaling showed involvement in regulating miR-301a-promoted cardiomyocyte differentiation from mES cells. CONCLUSION MiR-301a is capable of promoting embryonic stem cell differentiation to cardiomyocytes. |
资助项目 | National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81800243]; Science and Technology Commission of Shanghai MunicipalityScience & Technology Commission of Shanghai Municipality (STCSM) [18411965900]; Fundamental Research Funds for the Central UniversitiesFundamental Research Funds for the Central Universities [22120180125] |
出版者 | BAISHIDENG PUBLISHING GROUP INC |
出版地 | PLEASANTON |
ISSN | 1948-0210 |
卷号 | 11期号:12页码:1130-1141 |
DOI | 10.4252/wjsc.v11.i12.1130 |
页数 | 12 |
WOS类目 | Cell & Tissue Engineering ; Cell Biology |
WOS研究方向 | Cell Biology |
WOS记录号 | WOS:000512755700007 |
收录类别 | SCIE ; PUBMED ; SCOPUS |
URL | 查看原文 |
Pubmed记录号 | 31875873 |
PMC记录号 | PMC6904867 |
Scopus记录号 | 2-s2.0-85076777353 |
通讯作者地址 | [Yu, Zuo-Ren]Key Laboratory of Arrhythmias of the Ministry of Education of China,Tongji University School of Medicine,Shanghai,200120,China |
scopus学科分类 | Histology;Molecular Biology;Genetics;Genetics (clinical);Cell Biology |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | https://kms.wmu.edu.cn/handle/3ETUA0LF/5973 |
专题 | 检验医学院(生命科学学院、生物学实验教学中心)_病原生物学与免疫学系 基础医学院(机能实验教学中心)_病原生物学与免疫学系 |
通讯作者 | Yu, Zuo-Ren |
作者单位 | 1.Key Laboratory of Arrhythmias of the Ministry of Education of China,Tongji University School of Medicine,Shanghai,200120,China; 2.Research Center for Translational Medicine,Shanghai East Hospital,Tongji University School of Medicine,Shanghai,200120,China; 3.Department of Microbiology and Immunology,Wenzhou Medical College,Wenzhou, Zhejiang Province,325000,China |
推荐引用方式 GB/T 7714 | Zhen, Li-Xiao,Gu, Yu-Ying,Zhao, Qian,et al. MiR-301a promotes embryonic stem cell differentiation to cardiomyocytes[J]. WORLD JOURNAL OF STEM CELLS,2019,11(12):1130-1141. |
APA | Zhen, Li-Xiao., Gu, Yu-Ying., Zhao, Qian., Zhu, Hui-Fang., Lv, Jin-Hui., ... & Yu, Zuo-Ren. (2019). MiR-301a promotes embryonic stem cell differentiation to cardiomyocytes. WORLD JOURNAL OF STEM CELLS, 11(12), 1130-1141. |
MLA | Zhen, Li-Xiao,et al."MiR-301a promotes embryonic stem cell differentiation to cardiomyocytes".WORLD JOURNAL OF STEM CELLS 11.12(2019):1130-1141. |
条目包含的文件 | 下载所有文件 | |||||
文件名称/大小 | 文献类型 | 版本类型 | 开放类型 | 使用许可 | ||
WJSC201912007.CAJ(3335KB) | 期刊论文 | 出版稿 | 开放获取 | CC BY-NC-SA | 浏览 下载 |
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。
修改评论