Endometriosis stromal cell with estrogen
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ABSTRACT:
PROVIDER: PRJNA1198890 | ENA |
REPOSITORIES: ENA
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Project description:Objective : To compare transcriptomes induced by the estrogen components of combined oral contraceptives, estetrol (E4), and ethynylestradiol (EE), and estradiol (E2) in human primary endometriotic stromal cells (ESCs). Design: ESCs were cultured in the presence of E4 (10-6 mol/L), E2 (10-8 mol/L) or EE (10-9 mol/L) for 24 hours. The transcriptomes induced by E4 were compared with those by E2 and EE. Subjects: ESCs were obtained from patients with ovarian endometriomas. Main Outcome Measures: Comprehensive transcriptomes were examined using RNA sequencing analysis. mRNA levels were measured using reverse transcription and quantitative polymerase chain reaction (RT-qPCR) analysis. Results: E4 treatment resulted in 114 differentially expressed genes compared to the control (|log2fold change| >0.2). Within these genes, 79% (90 genes) changed in the same manner as with EE and E2. Of these genes, the expression levels of GREB1, PGR and BMP6 were validated using RT-qPCR analysis. In contrast, 21% (24 genes) changed in E4-preferential manner. Of these genes, FAM72A and ENSG00000280800 were validated using RT-qPCR analysis. Conclusion: Our results showed that the effect of E4 on ESC gene expression generally similar to those caused by EE and E2 but differed for some genes. This study will advance our understanding of combined oral contraceptives that have practical importance for the treatment of endometriosis.
2025-07-22 | GSE284362 | GEO
Project description:Gene expression profiling of primary stromal cell cultures isolated from human endometrium and ovarian endometriosis. Samples are derived from the endometrium of 6 healthy patients and the endometriomas of 6 diseased patients. The results indicate the gene expression differences between these two cell populations. Stromal cells were obtained from human normal endometrial tissues and ovarian endometriomas. The tissues were digested enzymatically, and pure stromal cell populations were established.
2014-08-01 | E-GEOD-58178 | biostudies-arrayexpress
Project description:Endometriosis is an estrogen-dependent inflammatory disease. A pivotal contributor to endometriosis is the estrogen receptor beta (ERβ), which drives the condition by impeding cell death through interferon (IFN) signaling. One noteworthy component of this cascade is the N-myc and STAT Interactor (NMI), an interferon alpha (IFNα) target gene whose expression is repressed in endometriotic lesions compared to normal endometrium. This repression is particularly pronounced in stromal cells, mediated by ERβ. The results of Western blot analyses, comparing IFNα-treated and untreated cells, demonstrate that IFNα treatment triggers cell death signaling, including apoptosis and necroptosis, in endometrial stromal cells. Intriguingly, NMI knockdown (KD) obstructed IFNα-induced cell death signaling in human endometrial stromal cells. Moreover, NMI KD amplified non-canonical IFNα pathways, such as β-Catenin/GSK3β and PI3K/AKT signaling, in endometrial stromal cells following IFNα treatment. RNA sequencing analyses unveiled that NMI KD augmented the expression of genes responsible for cell-cell adhesion and extracellular structural organization in IFNα-independent manners. These findings suggest that NMI KD plays an indispensable role in enhancing the adhesion and invasion of endometriotic cells during endometriosis progression. In summary, NMI functions as an endometriosis suppressor gene in endometriotic stromal cells, curbing the advancement of endometriosis. This intricate interplay of ERβ, IFNα signaling, and NMI offers novel insights into the mechanisms governing endometriosis development.
2025-08-31 | GSE241751 | GEO
Project description:Gene expression profiling of primary stromal cell cultures isolated from human endometrium and ovarian endometriosis. Samples are derived from the endometrium of 6 healthy patients and the endometriomas of 6 diseased patients. The results indicate the gene expression differences between these two cell populations.
2014-08-01 | GSE58178 | GEO
Project description:Background Reduced endometrial receptivity is a major factor for impaired fertility in endometriosis (EMS). Endometrial deposition of collagen I proteins may account for poor endometrial receptivity in endometriosis. Methods We investigated the expression of collagen I expression in endometrium of endometriosis patients and in constructed EMS mice model. Effect of collagen I on ESCs was evaluated. Co-culture of exosomes with ESCs was conducted to evaluate the uptake of exosomes by different endometrial cell lines and the effect on decidualization of eutopic ESCs and embryo implantation. MiRNA expression profiles were compared between ectopic ESC derived exosomes and eutopic ESC derived exosomes. Luciferase reporter and its mutant plasmids were applied to confirm the direct target of miR-25-3p. Findings Here we found endometrial collagen I deposition with impaired decidualization in endometriosis patients and EMS mice model. Treatment of collagen I with ESCs contributed to impaired decidualization and inhibited BLS expansion in vitro. Endometriotic stromal cell-derived exosomes were detected in eutopic endometrium and the ectopic endometrial stromal cell derived exosomes were more taken-up by the same cell line in eutopic endometrium. Treatment of endometriotic stromal cell-derived exosomes increased the expression of endometrial collagen I in vitro and in vivo, while inhibited BLS expansion. Exosomal miR-25-3p was significantly increased in endometriotic stromal cell-derived exosomes compared with control group, and PTEN is a certain target of miR-25-3p. The promotion of endometrial miR-25-3p significantly increased collagen I expression in vitro through the PTEN/Akt pathway. Interpretation These results suggested that endometriotic stromal cell-derived exosomal miR-25-3p played key role in inducing endometrial collagen I deposition to impair embryo expansion in endometriosis via PTEN/Akt pathway. Funding National Nature Science Foundation of China (82271702), National Natural Science Foundation of China (81771537). Keywords: endometriosis; exosome; collagen I; miRNA; collagen deposition
2025-01-28 | GSE222432 | GEO
Project description:We profiled transcriptomes of >370,000 individual cells from endometriomas (n=8), endometriosis (n=28), eutopic endometrium (n=10), unaffected ovary (n=4) and endometriosis-free peritoneum (n=4) to create a cellular atlas of endometrial-type epithelial cells, stromal cells, and microenvironmental cell populations across tissue sites.
2022-10-11 | GSE213216 | GEO
Project description:Estrogen receptor beta promotes endometriosis progression by up-regulating CD47 expression in ectopic endometrial stromal cells
| PRJNA714537 | ENA
Project description:Gene expression profiling of hormone treated normal and endometriosis stromal fibroblast cells (eSF). We used Affymetrix Human Gene 1.0 ST arrays. Samples include 4 normal of no uterine pathology (NUP), 4 endometriosis stage I, 4 endometriosis stage IV samples, each treated with Estrogen (E2), Progesterone (P4), E2+P4, or vehicle (veh), for a total of 48 samples on the Affymetrix platform.
2020-02-21 | GSE145701 | GEO
Project description:Genome-wide DNA methylation profiling of hormone treated normal and endometriosis stromal fibroblast cells (eSF). The Illumina Infinium Methylation BeadChip array 450 (HM450) was used. Samples include 4 normal of no uterine pathology (NUP), 4 endometriosis stage I, 4 endometriosis stage IV samples, each treated with Estrogen (E2), Progesterone (P4), E2+P4, or vehicle (veh), for a total of 48 samples analyzed on HM450.
2020-02-22 | GSE130028 | GEO
Project description:We primary cultured ectopic endometrial cells from patients with endometriosis (2 cases) and without endometriosis(2 cases) and collected cell culture supernatants（P0). We isolated exosomes from cell culture supernatants by differential centrifugation and then performed proteome analysis on the two groups of exosomes to investigate the role of ectopic endometrial cell-derived exosomes in the development of endometriosis.
2022-06-09 | PXD033124 | Pride