BMC veterinary research · 2025
Participation of COX2/mPGES1/PGE2 in mouse and human endometrial stromal decidualization.
СтатьяНазвание и аннотация: Перевод в очереди
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Wang Peng-Chao, Liu Jie, Liu Yue-Fang, Wu Yang, Xue Lin-Li, Yang Zhen-Shan
Аннотация
BACKGROUND: Prostaglandin E2 (PGE2) is vital for embryo implantation and decidualization. Whether COX2/mPGES1/PGE2 pathway is essential for mouse and human decidualization remains unclear.
RESULTS: This study showed that mPGES1 was highly expressed in the mouse uterus's subluminal stromal cells at the implantation site. COX2-specific inhibitor Valdecoxib and mPGES1 selective inhibitor MK886 were used to analyze the roles of mPGES1 and COX2 during mouse and human decidualization. During mouse in vitro decidualization, decidua/trophoblast prolactin-related protein (Dtprp) expression was significantly suppressed by Valdecoxib and MK886. Under human in vitro decidualization, mPGES1 significantly increases, while both cPGES and mPGES2 remain unchanged. PGE2-mediated upregulation of insulin growth factor binding protein 1 (IGFBP1) was significantly inhibited by Valdecoxib and MK886.
CONCLUSIONS: Our findings suggest the involvement of COX2/mPGES1/PGE2 pathway in both mouse and human decidualization.
RESULTS: This study showed that mPGES1 was highly expressed in the mouse uterus's subluminal stromal cells at the implantation site. COX2-specific inhibitor Valdecoxib and mPGES1 selective inhibitor MK886 were used to analyze the roles of mPGES1 and COX2 during mouse and human decidualization. During mouse in vitro decidualization, decidua/trophoblast prolactin-related protein (Dtprp) expression was significantly suppressed by Valdecoxib and MK886. Under human in vitro decidualization, mPGES1 significantly increases, while both cPGES and mPGES2 remain unchanged. PGE2-mediated upregulation of insulin growth factor binding protein 1 (IGFBP1) was significantly inhibited by Valdecoxib and MK886.
CONCLUSIONS: Our findings suggest the involvement of COX2/mPGES1/PGE2 pathway in both mouse and human decidualization.