Endometrial gland secretome maintains the homeostasis of decidualization
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ABSTRACT:
PROVIDER: PRJNA1297582 | ENA |
REPOSITORIES: ENA
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Project description:Decidualization of human endometrial stromal cells (hESCs), a critical process for embryo implantation and successful pregnancy, begins during the secretory phase of the menstrual cycle. We evaluated 25 established in vitro decidualization markers in hESCs using in vivo single-cell transcriptomic data. Most markers, including PRL and IGFBP1, did not reliably distinguish between proliferative and secretory phase hESCs, nor between decidualized and non-decidualized hESCs. Only 8 genes (STAT3, CEBPB, WNT4, IL-15, TIMP3, HAND2, FOXO1 and MMP19) showed differential expression between the menstrual phase and decidualization status in vivo. We hypothesized that the difference between in vitro and in vivo marker expression might result from the absence of endometrial glands in the in vitro decidualization model. While endometrial glands are known to secrete factors critical for uterine receptivity, their specific role in decidualization is not well understood. To investigate this, we examined the influence of the glandular secretome on ESC decidualization using an in vitro co-culture model of human endometrial organoids (hEOs) and hESCs. Decidualization was induced in hESCs, and the effects of hEO co-culture or exposure to hEO secretome were assessed by morphological analysis, molecular marker expression, and transcriptomic profiling. Unexpectedly, both hEO co-culture and exposure to the hEO secretome significantly reduce the up-regulation of canonical decidualization markers and the mesenchymal-epithelial transition typically induced during hESC decidualization. Transcriptomic analysis further revealed downregulation of decidualization regulators, CEBPA and EDN1, in ESCs exposed to the hEO secretome compared to decidualized controls. These findings were corroborated in an estradiol-stimulated mouse model, where increased endometrial gland formation correlated with reduced decidualization and lower expression of CEBPA and EDN1. Collectively, our results reveal a previously unrecognized homeostatic role for the endometrial gland secretome in regulating ESC decidualization. These insights highlight the limitations of current in vitro decidualization models and underscore the importance of glandular-stromal interactions in endometrial function and reproductive health.
2025-08-05 | GSE303741 | GEO
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: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.
2022-06-06 | GSE205084 | GEO
Project description:Endometrial gland impacts on stromal cell decidualization
| PRJNA843696 | ENA
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:The objectives of the present study were to determine whether obesity impacts human decidualization and the endometrial control of trophoblast invasion (both of which are required for embryo implantation) and evaluate the potential involvement of endometrial extracellular vesicles (EVs) in the regulation of these physiological processes. Using primary human cell cultures, we first demonstrated that obesity is associated with significantly lower in vitro decidualization of endometrial stromal cells (ESCs). We then showed that the trophoblastic cell line’s invasive ability was greater in the presence of conditioned media from cultures of ESCs from obese women. Using mass-spectrometry-based quantitative proteomics, we found that EVs isolated from uterine supernatants of biopsies from obese women (vs. nonobese women) presented a molecular signature focused on cell remodeling and angiogenesis. Lastly, the results of functional assays indicated that supplementation of the culture medium with EVs from nonobese women can rescue (at least in part) the defect in in vitro decidualization described in ESCs from obese women. Lastly, the addition of endometrial EVs from obese women (vs. nonobese women) was associated with significantly greater invasive activity by HTR-8/SVneo cells. In conclusion, our results provided new insights into the endometrial EVs’ pivotal role in the poor uterine receptivity observed in obese women.
2023-10-09 | PXD039568 | Pride
Project description:Timecourse of cAMP-induced decidualization of endometrial stromal cells.<br><br>Note that files GSM5962.txt and GSM5965.txt as imported from GEO are identical.
2007-12-13 | E-GEOD-403 | biostudies-arrayexpress
Project description:The zinc-finger transcription factor GATA2 has been shown to be important for endometrial stromal cell decidualization in early pregnancy in mice and humans. Progesterone and its receptor PGR is also critical during decidualization but its interaction with GATA2 in regulating genes and pathways necessary for decidualization in human endometrium are unclear. Human endometrial stromal cells were isolated from 5 premenopausal women for primary cell culture. The cells underwent in vitro decidualization (IVD) or vehicle (Veh) treatment for 10 days. RNA-sequencing (RNA-seq) was performed to compare gene expression profiles (n=3) and chromatin immunoprecipitation followed by sequencing (ChIP-seq) using an antibody against GATA2 (n=2) was performed to examine binding to target genes in the Veh and IVD cells. A public PGR ChIP-seq dataset (GSE69539) was mined to identify PGR-binding regions in IVD-treated human endometrial cells.
2020-02-22 | GSE145673 | GEO
Project description:The zinc-finger transcription factor GATA2 has been shown to be important for endometrial stromal cell decidualization in early pregnancy in mice and humans. Progesterone and its receptor PGR is also critical during decidualization but its interaction with GATA2 in regulating genes and pathways necessary for decidualization in human endometrium are unclear. Human endometrial stromal cells were isolated from 5 premenopausal women for primary cell culture. The cells underwent in vitro decidualization (IVD) or vehicle (Veh) treatment for 10 days. RNA-sequencing (RNA-seq) was performed to compare gene expression profiles (n=3) and chromatin immunoprecipitation followed by sequencing (ChIP-seq) using an antibody against GATA2 (n=2) was performed to examine binding to target genes in the Veh and IVD cells. A public PGR ChIP-seq dataset (GSE69539) was mined to identify PGR-binding regions in IVD-treated human endometrial cells.
2020-02-22 | GSE145671 | GEO
Project description:To identify the molecular pathway regulated by Scribble (SCRIB) in primary hunan endometrial stromal cells (ESCs) decidualization, high-throughput RNA-seq was performed to analyze the transcriptome profile in si-Ctrl or si-SCRIB transfected decidualized ESCs (dESCs).
2021-12-31 | GSE164331 | GEO