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A molecular mechanism of mouse placental spongiotrophoblast differentiation regulated by prolyl oligopeptidase

Published online by Cambridge University Press:  04 February 2019

Yuki Maruyama
Affiliation:
Graduate School of Life Science, Hokkaido University, Sapporo 060–0810, Japan
Atsushi P. Kimura*
Affiliation:
Graduate School of Life Science, Hokkaido University, Sapporo 060–0810, Japan Department of Biological Sciences, Faculty of Science, Hokkaido University, Sapporo 060-0810, Japan
*
*Address for correspondence: Atsushi P. Kimura. Department of Biological Sciences, Faculty of Science, Hokkaido University, Sapporo 060–0810, Japan. Tel: +81 11 706 4452. E-mail: akimura@sci.hokudai.ac.jp

Summary

In eutherian mammals, the placenta plays a critical role in embryo development by supplying nutrients and hormones and mediating interaction with the mother. To establish the fine connection between mother and embryo, the placenta needs to be formed normally, but the mechanism of placental differentiation is not fully understood. We previously revealed that mouse prolyl oligopeptidase (POP) plays a role in trophoblast stem cell (TSC) differentiation into two placental cell types, spongiotrophoblasts (SpT) and trophoblast giant cells. Here, we focused on SpT differentiation and attempted to elucidate a molecular mechanism. For Ascl2, Arnt, and Egfr genes that are indispensable for SpT formation, we found that a POP-specific inhibitor, SUAM-14746, significantly decreased Ascl2 expression, which was consistent with a significant decrease in expression of Flt1, a gene downstream of Ascl2. Although this downregulation was unlikely to be mediated by the PI3K-Akt pathway, our results indicated that POP controls TSC differentiation into SpT by regulating the Ascl2 gene.

Type
Short Communication
Copyright
© Cambridge University Press 2019 

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Footnotes

Cite this article: Y. Maruyama and A.P. Kimura (2019) A molecular mechanism of mouse placental spongiotrophoblast differentiation regulated by prolyl oligopeptidase. Zygote page 1 of 5. doi: 10.1017/S0967199418000655

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