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FOXO3a is essential for murine endometrial decidualization through cell apoptosis during early pregnancy.

Authors :
Long, Jing
Yang, Cheng‐Shun
He, Jun‐Lin
Liu, Xue‐Qing
Ding, Yu‐Bin
Chen, Xue‐Mei
Tong, Chao
Peng, Chuan
Wang, Ying‐Xiong
Gao, Ru‐Fei
Source :
Journal of Cellular Physiology. Apr2019, Vol. 234 Issue 4, p4154-4166. 13p.
Publication Year :
2019

Abstract

Embryo implantation is essential for normal pregnancy, and the process of decidualization is critical for embryo implantation. However, the mechanism of decidualization during early pregnancy is still unknown. Forkhead box O3a (FOXO3a) is the most important functional transcription factor of the forkhead box family and is a highly conserved transcription factor of apoptosis‐related genes. In the mouse uterus, FOXO3a was found to be expressed regularly from Days 1–7 of early pregnancy. Upon further exploration, it was found that FOXO3a was expressed at significantly higher levels at the implantation site than at the interimplantation site on Days 5–7 of pregnancy. Under artificial decidualization, FOXO3a was highly expressed in the first and second decidual zones. After decidualization, the expression of FOXO3a was significantly increased both in vivo and vitro. In primary stromal cells, apoptosis was reduced by decreased expression of FOXO3a after inducing decidualization. Moreover, when FOXO3a‐small interfering RNA was transfected into the uteri of mice, the expression of decidualization‐ and apoptosis‐related factors was impaired. Thus, FOXO3a might play an important role in decidualization during early pregnancy, and cell apoptosis might be one of pathways for FOXO3a‐regulated decidualization. Embryo implantation is essential for normal pregnancy, and the process of decidualization is critical for embryo implantation. The expression of forkhead box O3a (FOXO3a) was significantly increased when decidualization both in vivo and vitro. FOXO3a might play an important role in decidualization during early pregnancy. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00219541
Volume :
234
Issue :
4
Database :
Academic Search Index
Journal :
Journal of Cellular Physiology
Publication Type :
Academic Journal
Accession number :
133851191
Full Text :
https://doi.org/10.1002/jcp.27167