ArticleBMC veterinary research2025
Participation of COX2/mPGES1/PGE2 in mouse and human endometrial stromal decidualization.
Article in BMC veterinary research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Prostaglandin E2-mediated aging microenvironment fuels pathogenic fibrosis in cesarean section scar defect.EMBO molecular medicine · 2026Article
- Progesterone receptor isoform modulation via enhancer activation regulates progesterone signaling in endometrial stromal cells.F&S science · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundProstaglandin E2 (PGE2) is vital for embryo implantation and decidualization. Whether COX2/mPGES1/PGE2 pathway is essential for mouse and human decidualization remains unclear.
resultsThis 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.
conclusionsOur findings suggest the involvement of COX2/mPGES1/PGE2 pathway in both mouse and human decidualization.
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Registered trials
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