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Effect of BMP–Wnt–Nodal signal on stem cell differentiation

Published online by Cambridge University Press:  28 June 2021

Liyun Wang
Affiliation:
Guangzhou Huadu Maternal and Child Health Hospital, Guangzhou, Guangdong, China
Ronghua Ma
Affiliation:
Qinghai Provincial People’s Hospital, Xining, Qinghai, China
Gongxue Jia
Affiliation:
Northwest China institute of Plateau Biology, Xining, Qinghai, China
Shengyan Jian
Affiliation:
Qinghai Provincial People’s Hospital, Xining, Qinghai, China
Xianghui Zeng
Affiliation:
Qinghai Provincial People’s Hospital, Xining, Qinghai, China
Zhengfang Xiong*
Affiliation:
Qinghai Provincial People’s Hospital, Xining, Qinghai, China
Binye Li
Affiliation:
Qinghai Provincial People’s Hospital, Xining, Qinghai, China
Chen Li
Affiliation:
Qinghai Provincial People’s Hospital, Xining, Qinghai, China
*
*Author for correspondence: Zhengfang Xiong. Qinghai Provincial People’s Hospital, Xining, Qinghai, China. Email: [email protected]

Summary

The generation of germ cells from embryonic stem cells in vitro has current historical significance. Western blot, qPCR, immunofluorescence and flow cytometry assays were used to investigate the differences in expression levels of totipotency and specific markers for Wnt regulation and the related signalling pathways during primordial germ cell-like cell (PGCLC) induction and differentiation. During PGCLC induction, activation of WNT3a increased the expression of NANOG, SOX2 and OCT4, but Mvh, DAZL, Blimp1, TFAP2C, Gata4, SOX17, EOMES, Brachyury and PRDM1 expression levels were significantly reduced. Inhibition of the WNT signal demonstrated the opposite effect. Similarly, inhibitors of BMP and the Nodal/Activin signal were used to determine the effect of signal pathways on differentiation. CER1 affected the Wnt signal and differentiation, but the inhibitor SB only regulated differentiation. BMP–WNT–NODAL were mainly responsible for regulating differentiation. Our results provide a reliable theoretical basis and feasibility for further clinical medical research.

Type
Research Article
Copyright
© The Author(s), 2021. Published by Cambridge University Press

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