MiR-301a promotes embryonic stem cell differentiation to cardiomyocytes

• Published in: World journal of stem cells 2019-12, Vol.11 (12), p.1130-1141
• Main Authors: Zhen, Li-Xiao, Gu, Yu-Ying, Zhao, Qian, Zhu, Hui-Fang, Lv, Jin-Hui, Li, Shu-Jun, Xu, Zhen, Li, Li, Yu, Zuo-Ren
• Format: Article
• Language: English
• Subjects: Basic Study
• ISSN: 1948-0210; 1948-0210
• DOI: 10.4252/wjsc.v11.i12.1130

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. 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. 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 α-actinin were used to determine cardiomyocyte differentiation from mES cells. 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. 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. MiR-301a is capable of promoting embryonic stem cell differentiation to cardiomyocytes.