Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA892255 | ENA |
REPOSITORIES: ENA
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Project description:Proper decidualization is vital in preparation for a potential embryo receptivity, placentation, menstrual health and subsequent endometrial regeneration. Given the importance of extracellular vesicles (EVs) in intercellular communication, and recently in embryo implantation and indicators of menstrual cycle and fertility, we investigated their role during decidualization. Overall, this study provides an insight into distinct variation in sEV composition depending upon the level of decidualization of endometrial stromal cells, with the signaling potential to coordinate endometrial health ranging from embryo implantation, facilitating placentation and subsequent endometrial regeneration.
2021-11-17 | PXD026342 | Pride
Project description:Recurrent implantation failure (RIF) presents a significant challenge in the field of assisted reproductive technology, primarily stemming from compromised decidualization that impacts endometrial receptivity. Despite ongoing research efforts, the comprehensive molecular regulatory mechanisms involved in RIF remain incompletely understood. This study revealed significantly reduced levels of secretoglobin, family 2A, member 1 (SCGB2A1) in both the mid-secretory endometrium and uterine fluid of RIF patients compared to control subjects. Besides, combined with RNA sequencing results, we demonstrated that the suppression of SCGB2A1 results in reduced cell proliferation and impaired decidualization by modulating CDK3 signaling during cell cycle transition in immortalized human endometrial stromal cells (T-HESCs) and primary HESCs. Furthermore, our findings indicated that inhibition of endometrial SCGB2A1 in a rat model hinders embryo implantation and disrupts decidualization. In conclusion, this study provides evidence that SCGB2A1 serves as a novel biomarker for endometrial receptivity and plays a crucial role in the regulation of human endometrial decidualization. The findings offer valuable insights into the pathogenesis of decidualization-related RIF and have the potential to enhance strategies for improving pregnancy outcomes.
2025-01-01 | GSE269408 | GEO
Project description:Proper decidualization is a critical determinant of pregnancy success. Deficiencies in decidualization are associated with a variety of pregnancy disorders, including female infertility, recurrent implantation failure, and miscarriage. However, the mechanism for triggering decidualization of human endometrium is largely unknown. Here we characterized the transcriptomes of four major cells in human endometrium and decidua at single-cell resolution. We discovered the dynamic change characteristics of six major stromal cells. More importantly, a dialogue between IGF1+ stromal cells and IGF1R+ stromal cells initiates endometrial decidualization under regulation of progesterone and estrogen, and IL1B+ stromal cells trigger the apoptosis of epithelial cells and functional remodeling during decidualization. We defined a unique AREG+ NK cell for accelerating decidualization by interacting with IGF1+ stromal cells, and observed that extravillous trophoblasts promote decidualization possibly by multiply pathways. Additionally, we developed a systematic repository of cell-cell communication for decidualization via the ligand-receptor complexes interactions. Our study provides deeper insights into the molecular and cellular characterizations during decidualization.
2022-11-24 | GSE194219 | GEO
Project description:SCGB2A1 deficiency impairs endometrial stromal cell decidualization by decreasing CDK3-mediated proliferation in patients with recurrent implantation failure
| PRJNA1121401 | ENA
Project description:Uterine glands and, by inference, their secretions impact uterine receptivity, blastocyst implantation, stromal cell decidualization, and placental development. Changes in gland function across the menstrual cycle are impacted by steroid hormones, estrogen and progesterone, as well as stroma-derived factors. Using an endometrial epithelial organoid (EEO) system, transcriptome and proteome analyses identified distinct responses of the EEO to steroid hormones and prostaglandin E2 (PGE2). Notably, steroid hormones and PGE2 modulated the basolateral secretion of EEO proteins, where cystatin C (CST3) was significantly increased by progesterone and PGE2. CST3 treatment of decidualizing stromal cells significantly decreased the decidualization markers PRL and IGFBP1. The attenuation of stromal cell decidualization via CST3 suggests a role for uterine gland-derived proteins in controlling the extent of decidualization. These findings provide evidence that uterine gland-derived factors directly impact stromal cell decidualization, which has strong implications for better understanding pregnancy establishment and female fertility in humans.
2023-10-11 | PXD034357 | Pride
Project description:Decidualization is critical for the embryonic implantation and successful pregnancy. ATRA can suppress in-vitro decidualization of human endometrial stromal cells (hESCs) induced by MPA and estrogen treatment. However, the mechanism by which RA suppressed estrogen and progesterone induced decidualization of mESCs is not clear. We used microarrays to investigate the mechanism by which all-trans RA (ATRA) regulates the decidualization of endometrial stroma cells (mESCs). mESCs were isolated at day 4 of pseudopregnancy and cultured with administration of E2 and P4 in the presence or absence of ATRA for 72h.
2013-11-05 | E-GEOD-52033 | biostudies-arrayexpress
Project description:Our findings establish a key role for the coregulator, Repressor of Estrogen receptor Activity (REA), in controlling the timing and magnitude of decidualization in human endometrial stromal cells in vitro and in the mouse uterus in vivo, and suggest that REA functions to synchronize uterine differentiation with concurrent embryo development, which is essential for optimal implantation and fertility. The findings highlight that REA physiologically restrains endometrial stromal cell decidualization, controlling the timing and magnitude of decidualization to enable proper synchronization of uterine differentiation with concurrent embryo development that is essential for implantation and optimal fertility.
2013-04-04 | GSE42376 | GEO
Project description:Decidualization is critical for the embryonic implantation and successful pregnancy. ATRA can suppress in-vitro decidualization of human endometrial stromal cells (hESCs) induced by MPA and estrogen treatment. However, the mechanism by which RA suppressed estrogen and progesterone induced decidualization of mESCs is not clear. We used microarrays to investigate the mechanism by which all-trans RA (ATRA) regulates the decidualization of endometrial stroma cells (mESCs).
2013-11-05 | GSE52033 | GEO
Project description:To evaluate differentially expressed circRNAs in patients with recurrent implantation failure, we used circRNA microarrays to screen circRNA expression profiles in endometrial biopsies from 6 women with recurrent implantation failure and controls. Our study revealed for the first time a unique set of circRNA expression signatures in the endometrial tissue of patients with repeated implantation failure, which may provide new molecular candidates for the diagnosis and clinical treatment of embryo implantation failure.
2022-08-28 | GSE212030 | GEO
Project description:Our findings establish a key role for the coregulator, Repressor of Estrogen receptor Activity (REA), in controlling the timing and magnitude of decidualization in human endometrial stromal cells in vitro and in the mouse uterus in vivo, and suggest that REA functions to synchronize uterine differentiation with concurrent embryo development, which is essential for optimal implantation and fertility. The findings highlight that REA physiologically restrains endometrial stromal cell decidualization, controlling the timing and magnitude of decidualization to enable proper synchronization of uterine differentiation with concurrent embryo development that is essential for implantation and optimal fertility. Human endometrial stromal cells (hESCs) were isolated from biopsies taken from the early proliferative stage endometrium of regularly cycling women on no hormonal medications. Cells were cultured in DMEM/F-12 mediumcontaining 5% charcoal stripped fetal bovine serum. To induce in vitro decidualization, hESCs were treated with a hormone cocktail containing 10 nM estradiol (E2), 1 μM progesterone (P4) and 0.5 uM 8-bromo-cAMP for up to 10 days, and media were changed every 48 h. For siRNA experiments, hESCs were transfected with REA siRNA or GL3 luciferase control siRNA following the Silent-Fect kit protocol. After 48 h of transfection, hESCs were exposed to the hormone cocktail for 24 hours or 96 hours of differentiation. key words; siRNA knock-down, hormone cocktail treatment
2013-04-04 | E-GEOD-42376 | biostudies-arrayexpress