Publications by authors named "Pei-Li Wu"

In Brief: Insufficient trophoblast invasion at the maternal-fetal interface contributes to abortion-prone pregnancy. Our study shows that decreased levels of IGFBP7 in unexplained recurrent spontaneous abortion (URSA) trophoblast cells inhibit MMP2 and Slug expression as well as trophoblast invasion, suggesting that IGFBP7 should be considered a potential therapeutic protein target in URSA.

Abstract: Insufficient trophoblast invasion at the maternal-fetal interface contributes to abortion-prone pregnancy.

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Article Synopsis
  • Endometriosis is a chronic, estrogen-driven condition characterized by the abnormal growth of ectopic stromal cells (ESCs), making the search for safer treatments essential, with extracellular vesicles (EVs) from umbilical cord mesenchymal stem cells (UC-MSCs) being a potential solution.
  • The study involved culturing UC-MSCs, extracting EVs, and using them to stimulate ESCs to assess changes in cell proliferation, invasion, and specific estrogen-related protein expressions such as SF-1, ERβ, and aromatase.
  • Results indicated that exposure to 120 μg/mL EVs significantly reduced the levels of cyclin D1 and MMP
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Endometriosis is an estrogen-dependent disease, and estrogen receptor 2 (ESR2) plays a critical role in the pathogenesis of ovarian endometriosis by promoting cell invasion. Yes-associated protein 1 (YAP1) plays suppressive roles in several types of tumors. However, the relationship between YAP1 and ESR2 is not fully understood.

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Purpose: Ovarian hyperstimulation syndrome (OHSS) is a serious complication of assisted reproductive technology (ART) treatment. However, there are limited data regarding the ability of the luteal GnRH antagonist cetrorelix to reduce the incidence of moderate and severe OHSS, and the mechanism remains unclear. Thus, we designed a study to assess the effectiveness of cetrorelix to prevent early moderate and severe OHSS in high-risk patients undergoing controlled ovarian stimulation for IVF/ICSI.

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Endometriosis is an estrogen-dependent disease. Farnesoid X receptor (FXR) activation has been shown to inhibit estrogen signaling in breast cancer and testicular tumors. However, the role of FXR in endometriosis is still poorly understood.

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Steroidogenic factor-1 (SF-1, encoded by NR5A1) and estrogen receptor beta (ERβ, encoded by ESR2), which are highly expressed in endometriotic stromal cells (ESCs), contribute to the pathogenesis of endometriosis, but the regulation mechanism remains largely unknown. Transcription factor 21 (TCF21) belongs to the helix-loop-helix (bHLH) family characterized by regulating gene expression via binding to E-box element. Here, we attempted to determine the molecular mechanism of TCF21 on SF-1 and ERβ expression in endometriosis.

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Unlabelled: Estrogen receptor beta (ERβ, encoded by ESR2 gene) and cytochrome P450 aromatase (encoded by CYP19A1 gene) play critical roles in endometriosis, and the levels of insulin-like growth factor-I (IGF-I) in the peritoneal fluid are significantly higher in patients with endometriosis compared with those in normal women. However, the effects and mechanisms of IGF-I on ERβ and aromatase expression remain to be fully elucidated. In this study, human endometriotic stromal cells (ESCs) and endometrial cells (EMs) derived from ovarian endometriomas and eutopic endometrial tissues.

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